Raisa N Kazi

University of Science Malaysia, Nibong Tebal, Pulau Pinang, Malaysia

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Publications (13)7.51 Total impact

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    ABSTRACT: α(1D)-adrenoceptors are involved in the genesis/maintenance of hypertension in spontaneously hypertensive rats (SHR). This study aims to investigate the role of α(1D)-adrenoceptors in the antinatriuretic and antidiuretic responses in SHR subjected to high sodium (SHRHNa) and normal sodium (SHRNNa) intake for six weeks. Renal inulin clearance study was performed in which the antinatriuretic and antidiuretic responses to phenylephrine were examined in the presence and absence of α(₁D)-adrenoceptors blocker BMY7378. Data, mean±S.E.M. were subjected to ANOVA with significance at p<0.05. Results show that feeding SHR for six weeks with high salt did not cause any change in blood pressure. SHRHNa had higher (all p<0.05) urine flow rate (UFR), fractional and absolute excretion of sodium (FE(Na) and U(Na)V) compared to SHRNNa. Phenylephrine infusion produced significant reduction in UFR, FE(Na) and U(Na)V in both SHRHNa and SHRNNa. The antidiuretic and antinatriuretic responses to phenylephrine in both groups were attenuated in the presence of BMY7378. Moreover, the antidiuretic and antinatriuretic responses to phenylephrine and BMY7378 were independent on any significant changes in renal and glomerular hemodynamics in both groups. Thus we conclude that high sodium intake did not bring any further increase in blood pressure of SHR, however, it results in exaggerated natriuresis and diuresis in SHRHNa. Irrespective of dietary sodium changes, α₁-adrenoceptors are involved in mediating the antinatriuretic and antidiuretic responses to phenylephrine in SHR. Further, high sodium intake did not significantly influence the functionality of α(₁D)-adrenoceptors in mediating the adrenergically induced antinatriuresis and antidiuresis.
    Yakugaku zasshi journal of the Pharmaceutical Society of Japan 03/2011; 131(3):431-6. · 0.46 Impact Factor
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    ABSTRACT: This study examined the effect of renal sympathetic innervation on adrenergically and angiotensin II (Ang II)-induced renal vasoconstriction in Wistar-Kyoto (WKY) rats. Forty-eight WKY rats were treated with either losartan (10 mg/kg/day p.o.) or carvedilol (5 mg/kg/day p.o.) or a combination of them (10 mg/kg/day + 5 mg/kg/day p.o.) for 7 days. On day 8, the rats were anaesthetized, and renal vasoconstrictor experiments were carried out. A group of rats was subjected to acute unilateral renal denervation during the acute study. Changes in the renal vasoconstrictor responses were determined in terms of reductions in renal blood flow caused by Ang II, noradrenaline (NA), and methoxamine (ME). In normal animals, losartan decreased (P < 0.05) the renal vasoconstrictor response to Ang II but not to NA or ME. Carvedilol treatment, however, blunted (P < 0.05) the renal vasoconstrictor responses to Ang II and adrenergic agonists. Combination of losartan and carvedilol blunted (P < 0.05) the renal vasoconstrictor response to Ang II but augmented the responses to NA and ME (all P < 0.05). Interestingly, when denervated rats were treated with the same combination, there was a reduction (P < 0.05) in the renal vasoconstrictor responses to Ang II and adrenergic agonists. Data suggest that the renal sympathetic nerve contributes to adrenergic agonist-mediated renal vasoconstrictions in normal rats. The data further indicate an interactive relationship between renin-angiotensin and sympathetic nervous systems in modulating adrenergically and Ang II-induced renal vasoconstriction in WKY rats.
    Upsala journal of medical sciences 11/2010; 116(1):18-25. · 0.73 Impact Factor
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    ABSTRACT: It is well established that renal sympathetic nerves are primarily involved in renal sodium and water regulation. However, the relationship between renal sympathetic nerve activity (RSNA) and renal potassium handling is not extensively known. The present study was performed to investigate the role of the renal sympathetic nervous system in the regulation of tubular potassium reabsorption and secretion. Male Sprague Dawley (SD) rats (each group, n=6) were fasted overnight, anesthetized with pentobarbital sodium (60 mg/kg intraperitoneal), denervated by application of phenol to the left renal artery and maintained on an intravenous infusion of saline for 2 hours. During this period, 6 urine and plasma samples were collected at 20-minute intervals to study kidney function parameters. In denervated rats, there were significantly higher (all p<0.05 vs. innervated control) urine flow rate (UFR), glomerular filtration rate (GFR), absolute sodium excretion (U(Na)V), fractional sodium excretion (FE(N)a), absolute potassium excretion (U(K)V), fractional potassium excretion (FE(K)) and urinary sodium to urinary potassium ratio (U(Na)/U(K)). No appreciable differences were seen in the mean arterial pressure (MAP) and plasma sodium (P(Na)) between denervated and innervated SD rats. However, plasma potassium (P(K)) levels were significantly lower (p<0.05) in denervated rats as compared with innervated counterparts. There is a possible involvement of renal nerves in the regulation of renal potassium handling. This effect is largely attributable to a direct action of renal sympathetic nerves on the renal tubular segments.
    Journal of nephrology 03/2010; 23(3):291-6. · 2.02 Impact Factor
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    ABSTRACT: Regulation of renal function and haemodynamics are under a direct control from the renal sympathetic nerves and renal denervation produces overt diuresis and natriuresis in several mammalian species. However, the inter-related series of changes in renal function and haemodynamics following acute renal denervation (ARD) is not fully understood. Thus, we aimed to investigate and relate the changes in renal function and haemodynamics following acute unilateral renal denervation in anaesthetized Sprague Dawley (SD) rats. Male SD rats were fasted overnight, anaesthetized with sodium pentobarbitone (60 mg/kg ip), denervated by application of phenol to the left renal artery and maintained on an intravenous (iv) infusion of isotonic saline for 2 h. Throughout this period, six urine and plasma samples were taken at 20-min intervals to study kidney function parameters. In a different set of experiments, renal nerve stimulation (RNS) was carried out to characterize the changes in renal vasoconstrictor responses following ARD. Denervated animals showed significantly (P<0.05 vs. control innervated rats) higher urine flow rate (UFR), absolute sodium excretion (UNaV), fractional sodium excretion (FENa) and glomerular filtration rate (GFR). The renal vasoconstrictor responses to RNS were significantly (P<0.05) lower in denervated rats as compared to the innervated counterparts. However, no appreciable differences were seen in the mean arterial pressure (MAP), plasma sodium (PNa), basal renal blood flow (RBF) and basal renal vascular resistance (RVR) in both innervated and denervated SD rats. Natriuresis, diuresis, enhanced GFR and impaired vasoconstriction in response to RNS are typical and instant responses to ARD in SD rats. Renal sympathetic nerves serve more important role in salt and water conservation than in dynamic autoregulation of RBF under normal sympathetic tone; yet, their effects on renal haemodynamics become more evident in the presence of augmented renal sympathetic nerve activity (RSNA).
    The Indian Journal of Medical Research 01/2010; 131:76-82. · 2.06 Impact Factor
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    Yakugaku zasshi journal of the Pharmaceutical Society of Japan 01/2010; 131:431-436. · 0.46 Impact Factor
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    ABSTRACT: Background. Elevated dietary sodium intake exacerbates the elevation of blood pressure in spontaneously hypertensive rats (SHR) which is associated with increased renal vascular resistance and fluid reabsorption. The renal sympathetic nerves exert their action via α1-adrenoceptors (α1-AR) with α1A as the major subtype in regulating renal hemodynamics and excretory function. Objectives. This study investigated whether the contribution of α1A-AR in regulating renal vasoconstriction and excretory function was enhanced in SHR receiving high sodium intake. Material and Methods. SHR received either water (SHRNNa) or normal saline (SHRHNa) for six weeks. Metabolic cage studies followed by acute experiments were carried out on these SHR to examine renal vasoconstrictor and excretory responses to catecholamine viz. noradrenaline (NA), phenylephrine (PE) and methoxamine (ME) in the presence and absence of a α1A-AR blocker, 5-methylurapidil (5-MeU). Results. Daily water intake and urine output were increased in SHRHNa (P < 0.05 vs. SHRNNa). Renal cortical vascular responses to NA, PE and ME were enhanced in SHRHNa (P < 0.05 vs. SHRNNa) and the greatest effect was seen with ME. Intra-renal infusion of PE caused antidiuresis and antinatriuresis. Irrespective of the sodium intake, 5-MeU markedly blunted adrenergically induced renal cortical vasoconstrictions in SHR, while the antinatriuretic and antidiuretic responses to PE were inhibited by 5-MeU in SHRHNA only (P < 0.05). Conclusions. The data suggest that, irrespective of the level of dietary sodium intake, α1A-ARs are the functional subtypes in SHR. However, there also appears to be a role for α1A-AR in mediating enhanced renal cortical vascular resistance, augmented tubular Na+ and water reabsorption in SHRHNa rats (Adv Clin Exp Med 2011, 20, 1, 47–55).
    Advances in Clinical and Experimental Medicine 01/2010; 20:47–55. · 0.09 Impact Factor
  • Kidney & Blood Pressure research. 10/2009; 32:349-359.
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    ABSTRACT: This study investigated the impact of hypertension combined with diabetic nephropathy on rat renal alpha(1)-adrenoceptor subtype composition. In streptozotocin-induced diabetic spontaneously hypertensive rats (SHR), diabetic nephropathy developed as reflected by increased kidney index, plasma creatinine, albumin excretion, creatinine clearance and fractional excretion of Na(+) (all p < 0.05). Renal vasoconstrictions caused by electrical stimulation of renal nerves and intrarenally administered noradrenaline (alpha-adrenoceptor agonist), phenylephrine (alpha(1)-adrenoceptor agonist) and methoxamine (alpha(1A)-adrenoceptor agonist) were determined in the presence and absence of intrarenally administered amlodipine (Ca(2+) channel blocker), 5-methylurapidil (alpha(1A)-adrenoceptor antagonist), chloroethylclonidine (alpha(1B)-adrenoceptor antagonist) and BMY 7378 (alpha(1D)-adrenoceptor antagonist). In diabetic nephropathy SHR, there was a significant (all p < 0.05) attenuation of all adrenergically induced vasoconstrictor responses in the antagonists, except chloroethylclonidine, which caused a significant (all p < 0.05) enhancement of the responses. The data demonstrated that there was a functional coexistence of alpha(1A)- and alpha(1D)-adrenoceptors in the renal vasculature of SHR irrespective of the presence of diabetic nephropathy. However, there was a minor contribution of pre-synaptic alpha-adrenoceptors to the adrenergically mediated vasoconstrictor responses in the diabetic nephropathy SHR.
    Kidney and Blood Pressure Research 10/2009; 32(5):349-59. · 1.60 Impact Factor
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    Advances in Clinical and Experimental Medicine 09/2009; 18:205-214. · 0.09 Impact Factor
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    ABSTRACT: The present study investigated the renal functional and hemodynamic changes in rats with very recent onset of type I diabetes mellitus (DM). Male Sprague Dawley rats were induced with experimental DM by an i.p. injection of 55 mg/kg streptozotocin (STZ). The diabetic state in rats was confirmed by hyperglycemia, polyuria, polydipsia and reduction in the body mass. Acute clearance and hemodynamic experiments were performed 7 d after the onset of DM. During the acute study, diabetic rats showed no marked alteration (all P>0.05 vs. control) in the urine flow rate (UFR). Both absolute (UNaV) and fractional (FENa) sodium excretions were significantly lower (all P<0.05 vs. control) in diabetic rats. Kidney glomerular filtration rate (GFR), plasma sodium (PNa) and plasma creatinine (PCr) were significantly higher in diabetics (all P<0.05 vs. control). Mean arterial pressure (MAP) and renal blood flow (RBF) were slightly higher while renal vascular resistance (RVR) was slightly lower; however, these changes were not significantly different from the control (all P>0.05). Kidney weight was only slightly higher in diabetic rats (P>0.05 vs. control) but no observable changes in renal histology were detected. These results suggest that acute renal insufficiency of a prerenal cause seems to accompany recent onset type I DM. The changes in kidney function, at least in part, are likely to be due to the associated volume depletion.
    Pharmacologyonline. 08/2009; 2.
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    ABSTRACT: 1 Increased renal vascular resistance is one renal functional abnormality that contributes to hypertension, and alpha(1)-adrenoceptors play a pivotal role in modulating this renal vascular resistance. This study investigates the functional contribution of alpha(1)-adrenoceptor subtypes in the renal cortical vasculature of Wistar-Kyoto rats on a normal sodium diet (WKYNNa) compared with those given saline to drink for 6 weeks (WKYHNa). 2 The renal cortical vascular responses to the adrenergic agonists noradrenaline (NA), methoxamine (ME) and phenylephrine (PE) were measured in WKYHNa and WKYNNa rats either in the absence (the control phase) or presence of chloroethylclonidine (CEC), an alpha(1B)-adrenoceptor antagonist, 5-methylurapidil (5-MeU), an alpha(1A) antagonist, or BMY7378, an alpha(1D) antagonist. 3 Results showed a greater renal cortical vascular sensitivity to NA, PE and ME in the WKYHNa compared with WKYNNa rats (P < 0.05). Moreover, 5-MeU and BMY7378 attenuated adrenergically induced renal cortical vasoconstriction in WKYHNa and WKYNNa rats; this response was largely blunted in CEC-treated WKYHNa rats (all P < 0.05) but not in CEC-treated WKYNNa rats. 4 The data suggest that irrespective of dietary sodium content, in Wistar-Kyoto rats alpha(1A)- and alpha(1D)-subtypes are the major alpha(1)-adrenoceptors in renal cortical vasculature; however, there appears to be a functional involvement of alpha(1B)-adrenoceptors in the WKYHNa rats.
    Autonomic &amp Autacoid Pharmacology 01/2009; 29(1-2):25-31.
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    ABSTRACT: It is well established that the sympathetic nervous system (SNS) plays a crucial role in the control of renal hemodynamics. This study was set out to study the contribution of renal sympathetic nerves and renin-angiotensin system (RAS) in the regulation of renal hemodynamics, in an attempt to investigate the interaction between SNS and RAS at the level of renal resistance vessel of normal Wistar-Kyoto (WKY) and Spontaneously Hypertensive rats (SHR) by examining the effect of acute unilateral renal denervation on the renal hemodynamic responses to a set of vasoactive agents. Forty-eight male WKY and SHR rats were subjected to acute unilateral renal denervation during the acute study and the changes in the renal vasoconstrictor responses were determined in terms of reduction in renal blood flow caused by intrarenal administration of bolus doses of noradrenaline, phenylephrine, methoxamine and angiotensin II. The data for both WKY and SHR rats showed that there was significantly (all P<0.05) increased renal vascular responsiveness to the vasoactive agents in denervated rats compared to those with intact renal nerves. In losartan treated denervated SHR rats, there were significant (all P<0.05) reductions in the renal vasoconstrictor responses to vasoactive agents as compared to that of untreated denervated SHR rats. In normal losartan treated rats, there was no significant change in the vasoconstrictor response when compared to their untreated counterparts except for angiotensin II (P<0.05). The data obtained in denervated rats suggested an enhanced sensitivity of the ?1-adrenoceptors to adrenergic agonists and possible increase in AT1-receptors in the renal vasculature of SHR rats. These data collectively reaffirm the fact that a1-adrenoceptor and post synaptic AT1-receptors are functionally important in the regulation of renal vasoconstriction in hypertensive rats and also suggested a possible interaction between SNS and RAS in terms of a crosstalk between renal AT1 and a1-adrenoceptor subtypes in pathological condition of hypertension.
    22nd Malaysian Society of Physiology and Pharmacology Scientific Meeting; 01/2008
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    ABSTRACT: Background. It is well known that the pathogenesis of most renal diseases is associated with alterations in renal hemodynamics and also that the regulation of renal hemodynamics is under the direct control of renal sympathetic nerve activity. Objectives. The role of the renal sympathetic nervous system in the early deterioration of renal hemodynamics in rats with pathophysiological states of renal impairment was investigated. Material and Methods. Male Sprague Dawley rats were induced with acute renal failure or diabetes mellitus by cisplatin or streptozotocin (STZ), respectively. Cisplatin−induced renal failure was confirmed by impaired renal function and the diabetic state and early renal impairment were confirmed by hyperglycemia, changes in physio− logical parameters, and renal function. The hemodynamic study was conducted on anesthetized rats 7 days after cisplatin or STZ administration. During the acute study the renal sympathetic nerves were electrically stimulated at increasing frequencies and the responses in renal blood flow (RBF) and renal vascular resistance (RVR) were recorded in the presence and absence of renal denervation. Results. In the innervated rats with renal impairment, renal nerve stimulation (RNS) caused significant attenuation (all P < 0.05 vs. innervated control) of the renal vasoconstrictor responses. These responses were markedly (all P < 0.05) abolished when renal denervation was performed; however, they appeared significantly (all P < 0.05) higher than the denervated control counterparts. Conclusions. The findings strongly suggest an early involvement of renal sympathetic nerve action in the patho− genesis of renal impairment accompanying renal failure and diabetes. The data further suggest an early enhance− ment of renal sensitivity to intrarenal norepinephrine upon the removal of renal sympathetic tone by denervation (Adv Clin Exp Med 2009, 18, 3, 205-214).