A H Werber

Michigan State University, Ист-Лансинг, Michigan, United States

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Publications (4)16.33 Total impact

  • A H Werber · W J Bryan · G D Fink
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    ABSTRACT: Experiments were performed to test the hypothesis that acute hypertension caused by aortic baroreceptor deafferentation (ABD) is the result of sympathetic vasoconstriction. Cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR) were measured before and after ABD in anesthetized and conscious rats. The role of the sympathetic nervous system in acute ABD-induced hypertension was evaluated by examining the ability of adrenalectomy, adrenal demedullation, guanethidine or combined adrenal demedullation, and guanethidine pretreatment to prevent, and total autonomic blockade to reverse, ABD-induced hypertension. CO did not change significantly after ABD at any time, whereas MAP and TPR increased significantly (P less than 0.05). Only combined adrenal demedullation and guanethidine pretreatment prevented ABD-induced hypertension, and autonomic blockade normalized MAP in ABD rats. Normalization of blood pressure was the result of a decreased TPR. It is concluded that acute ABD-induced hypertension results from vasoconstriction caused by neurally released and/or circulating catecholamines.
    No preview · Article · Jan 1985 · The American journal of physiology
  • G D Fink · W J Bryan · M Mann · J Osborn · A Werber
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    ABSTRACT: The purpose of this study was to determine if once-daily arterial pressure measurements are a reliable estimate of actual time-averaged arterial pressure in neurogenic hypertensive rats. Male rats were subjected to either aortic baroreceptor deafferentation (ABD, n = 10) or sham operation (SO, n = 10). One to 3 mo later, arterial pressure (AP) was recorded from a chronic indwelling catheter in each rat for 72 continuous hours. Subsequently, AP was determined once a day (10- to 30-min recording periods) in each rat for an additional 3 consecutive days. Continuous recording yielded an average mean arterial pressure (MAP) of 104 +/- 2 mmHg in SO rats and an average mean MAP of 120 +/- 3 mmHg in ABD rats. Standard deviation of MAP measured every 5 min for 24 consecutive hours (as an index of pressure lability) was 8.0 +/- 0.4 mmHg in SO rats and 14.4 +/- 1.3 mmHg in ABD rats. Both of the above differences were statistically significant (P less than 0.05). The average MAP from daily measurements in the same rats was 107 +/- 3 mmHg in SO rats and 124 +/- 3 mmHg in ABD rats. Average pressure values were not statistically different for the two measurement techniques in either group of rats. Overall, there existed a significant correlation (r = 0.64, P less than 0.01) between MAP measured continuously and daily in the 20 rats studied. We conclude that daily direct measurement of MAP in conscious ABD rats yields a satisfactory estimate of actual time-averaged MAP in these rats despite their markedly increased MAP lability.
    No preview · Article · Sep 1981 · The American journal of physiology
  • A H Werber · G D Fink
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    ABSTRACT: These experiments were performed to determine the role of fluid volume contraction in the compensatory cardiovascular response to an abrupt neurogenically mediated increase in systemic arterial blood pressure. Acute neurogenic hypertension was produced by selective aortic baroreceptor deafferentation (ABD) in the rat. Salt and water balance, fluid compartment volumes, and arterial pressure were measured before and for 5 days after the induction of hypertension by ABD. In rats with ABD, arterial pressure was increased approximately 30 mmHg 1 day after deafferentation and declined 15-20 mmHg over the next 4 days. Plasma volume and extracellular fluid volume were decreased 5 days after ABD. Urine output did not increase after ABD, and the fluid volume contraction was instead the result of a significant decrease in water intake. Sham-operated rats did not exhibit significant changes in any of these parameters. Sodium balance decreased slightly in both sham-operated and ABD rats postsurgery. These results confirm that fluid volume contraction is a prominent compensatory response to an abrupt rise in arterial pressure, but suggest that this compensation is not necessarily mediated through alterations in renal salt and water excretion.
    No preview · Article · Jun 1981 · The American journal of physiology
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    G D Fink · F Kennedy · W J Bryan · A Werber
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    ABSTRACT: In an attempt to produce a form of chronic neurogenic hypertension without the increased blood pressure lability which is characteristic of total baroreceptor removal, selective aortic baroreceptor deafferentation (ABD) was performed in rats. Blood pressure, blood pressure variability, heart rate, plasma and extracellular fluid volumes, and the effect of total autonomic blockade were determined in male rats 1 month following ABD. Rats with ABD had significantly higher systolic, diastolic, and mean arterial blood pressures than did sham-operated animals, but the standard deviation of pressure measured repetitively over a 1-hour period was not significantly greater. Total autonomic blockade with atropine, propranolol, and phentolamine lowered blood pressure and heart rate to a similar level in ABD and sham-operated rats. Extracellular fluid volume was not different in the two groups of rats, but plasma volume was significantly lower in rats with ABD. Despite the overall reduction in plasma volume, there was a significant positive correlation between plasma volume and blood pressure in ABD rats; no such correlation was observed in sham-operated rats. It was concluded that ABD produces a mild, chronic hypertension in rats without marked pressure lability. Although the hypertension appears to be Neurogenic in that it is ABOLIshed by autonomic blockade, volume factors also may contribute to the increased blood pressure.
    Preview · Article · May 1980 · Hypertension