SUMMARY. To determine the influence of vasopressin on baroreceptor reflex mechanisms, baroreflex function in Brattleboro rats was compared with that in normal Long-Evans rats. Baroreflex function was assessed in conscious unrestrained rats during increases in blood pressure with phenylephrine (200 Mg/kg per min for 10 seconds). The baroreflex function line was obtained by plotting the log (pulse period) against the preceding systolic pressure on a beat-by-beat basis. The slope of the baroreflex function line (baroreflex function slope) in Long-Evans rats [(19.0 ± 1.4) X 10" 4 , mean ± SEM, n = 34] was significantly steeper than that in Brattleboro rats [(6.9 ± 0.6) X 10~\ n = 44, P < 0.001]. A subpressor intravenous infusion of arginine 8 -vasopressin (2 ng/kg per min for 2 hours), which elevated plasma vasopressin to 48.1 ± 6.8 pg/ml, caused bradycardia and increased the baroreflex function slope in Brattleboro rats, from (7.5 ± 1.0) x 10"" to within the normal Long-Evans range [(17.0 ± 0.8) x 10~\ n = 7, P < 0.001]. The basal pulse period and the baroreflex function slope in Brattleboro rats [(7.0 ± 0.9) x 10~4] was also increased significantly to (12.0 ± 1.7) X 10"* (n = 11, P < 0.01) by an infusion of l-desamino-8-D-arginine vasopressin, (2 ng/kg per min for 2 hours), a vasopressin analogue with potent antidiuretic but minimal vascular actions. Acute volume expansion, which increased body weight significantly, did not change the baroreflex function slope in Brattleboro rats [(7.7 ± 1.1) X 10" [140][141][142][143][144][145][146][147][148][149] 1983)
Studies were performed in anesthetized dogs to determine if the diuretic effect of clonidine results from inhibition of vasopressin secretion. Intravenous clonidine (30 microgram/kg) decreased plasma vasopressin concentration (as measured by RIA) from 10.9 +/- 1.5 to 5.0 +/- 1.1 ng/ml (P less than 0.01) in association with a transient increase in arterial blood pressure and a decrease in heart rate. Intravenous administration of two alpha-adrenoceptor antagonists, piperoxane and phentolamine, virtually abolished the pressor effect of clonidine but did not prevent the suppression of plasma vasopressin concentration. Clonidine decreased plasma vasopressin concentration from 11.9 +/- 3.1 to 3.3 +/- 1.0 pg/ml in the phentolamine-treated dogs (P less than 0.01) and from 18.1 +/- 4.5 to 12.4 +/- 3.6 pg/ml in the piperoxane-treated dogs (P less than 0.05). These results provide direct evidence that the diuretic effect of clonidine results from inhibition of the secretion of vasopressin. This inhibition does not appear to be a consequence of the pressor effect of the drug but may result from a direct action in the central nervous system.
SUMMARY The contribution of vasopressin and angiotensin II to the maintenance of blood pressure after short-term autonomic blockade was investigated in conscious Long-Evans and Brattleboro (vasoprcssin-deficient; hereditary diabetes insipidus) rats. After short-term autonomic blockade by atropine (1 mg/kg), propranolol (5 mg/kg), and pentolinium (5 mg/kg and 10 mg/kg/hr), the fall in blood pressure was significantly greater in Brattleboro rats than in Long-Evans rats (48 ± 3 vs 32 ± 2 mm Hg; p < 0.01). Administration of the vasopressin vascular receptor antagonist D(CH 2 ) 5 Tyr-(Me)AVP (2 /^g/kg) caused further blood pressure decreases only in Long-Evans rats, so that the final blood pressure in both groups was identical. Administration of enalaprilat (10 mg/kg), an angiotensin converting enzyme inhibitor, further reduced blood pressure in both strains. When enalaprilat was given first after autonomic blockade, it reduced blood pressure in Brattleboro rats but not in LongEvans rats. Administration of the vasopressin antagonist after enalaprilat further reduced blood pressure only in Long-Evans rats. The fall in blood pressure following vasopressin blockade was greater than that occurring after angiotensin converting enzyme inhibition (14 ± 1 vs 6 ± 1 mm Hg; p < 0.05) in autonomic blockaded Long-Evans rats. Plasma levels of vasopressin in Long-Evans rats increased markedly after short-term autonomic blockade, whereas plasma renin and angiotensin II levels were unchanged. Plasma angiotensin II levels were increased by the vasopressin antagonist and decreased by enalaprilat. We conclude that, due to sympathetic nervous system blockade and consequent blunting of renal renin release, vasopressin has a greater capacity than the renin-angiotensin system for maintaining blood pressure after short-term autonomic blockade. (Hypertension 7: 547-553, 1985) KEY WORDS • renin • Brattleboro rat • hypertension • hypotension • converting enzyme inhibition * vascular tone B LOOD pressure (BP) regulation is a multifactorial phenomenon involving numerous complex interactions.1 " 3 The three major pressor mechanisms influencing BP are the autonomic nervous system and the vasoactive peptides angiotensin and vasopressin. The importance of the autonomic nervous system in cardiovascular control mechanisms is well defined, and the role of the renin-angiotensin system in various physiological and hypertensive or hypotensive
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