Redundant nature of the vasopressin and rennin–angiotensin systems in the control of mesenteric resistance vessels of the conscious fasted cat

1983 ◽  
Vol 61 (7) ◽  
pp. 770-773 ◽  
Author(s):  
J. R. McNeill
Keyword(s):  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Enzyme Inhibitor ◽  
Mesenteric Arteries ◽  
The Other ◽  
Converting Enzyme ◽  
Plateau Phase ◽  
Resistance Vessels ◽  
Pressor Activity ◽  
Specific Antagonist

[1-deaminopenicillamine, 4-valine, 8-D-arginine]Vasopressin (DPVDAVP), a specific antagonist of the pressor activity of vasopressin, and teprotide, a converting enzyme inhibitor, were infused intravenously in conscious, fasted (24–30 h) but not water-deprived cats which had been implanted previously with flow probes on their superior mesenteric arteries and with arterial and venous cannulae. Infusion of DPVDAVP (20 μg/min) alone or teprotide (1 mg over 5 min) alone caused only small and statistically nonsignificant changes in mesenteric conductance and arterial pressure. However, infusion of DPVDAVP during the plateau phase of the response to teprotide or, conversely, administration of teprotide during the plateau phase of the response to DPVDAVP caused large increases in mesenteric conductance and small but significant decreases in arterial pressure. The results are consistent with the hypothesis that vasopressin and angiotensin are redundant overlapping mechanisms that play a significant role in the control of the mesenteric resistance vessels of the conscious fasted cat; when one system is inhibited, the other compensates to maintain resistance.

Prolonged inhibition of pressor response to vasopressin by a potent specific antagonist, [1-(β-mercapto-β,β-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]arginine-vasopressin

1981 ◽  
Vol 59 (9) ◽  
pp. 1008-1012 ◽  
Author(s):  
Catherine C. Y. Pang ◽  
Kenneth M. Leighton
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Duration Of Action ◽  
Pressor Responses ◽  
Anaesthetized Rats ◽  
Pressor Activity ◽  
Specific Antagonist

The specificity, the potency, and the duration of action of [1-(β-mercapto-β,β-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]arginine-vasopressin [d(CH2)5Tyr(Me)AVP] to antagonize pressor responses to arginine vasopressin (AVP) was examined in pentobarbital-anaesthetized rats. Injection of the compound (4 μg∙kg−1 i.v.) prevented pressor responses to i.v. infusions of supramaximal doses of AVP, but not to i.v. infusions of another peptide, angiotensin II (Ag II). The antagonism of AVP persisted for at least 3 h. Since i.v. injection of the compound in the absence of exogenous administration of AVP did not cause any change in the arterial pressure of rats, it appears that the compound is devoid of agonistic pressor activity. The results show that d(CH2)5Tyr(Me)AVP is a potent and a specific antagonist of pressor responses to AVP.

Comparison of pressor responses to angiotensin I, II, and III in pulmonary vascular bed of cats

1994 ◽  
Vol 266 (6) ◽  
pp. H2247-H2255
Author(s):  
D. Y. Cheng ◽  
B. J. DeWitt ◽  
T. J. McMahon ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Time Course ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Pulmonary Vasodilator ◽  
Pressor Responses ◽  
Pressor Activity ◽  
Ang Iv

Pulmonary vascular responses to angiotensin (ANG) peptides were investigated in the intact-chest cat under conditions of controlled blood flow and constant left atrial pressure. Intralobar injections of ANG I, II, and III caused dose-related increases in lobar arterial pressure, whereas ANG (1–7) and ANG (3–8) (ANG IV) had modest pressor activity. ANG I, II, and III had similar activity and were more potent than norepinephrine and ANG (1–7) and ANG IV but less potent than the thromboxane A2 mimic, U-46619, in increasing lobar arterial pressure. The time course of responses to ANG I, II, and III was similar, and after administration of ANG receptor antagonists, DuP 532 and L-158,809, responses to ANG I, II, and III was reduced, whereas responses to norepinephrine, serotonin, and U-46619 were not altered. After administration of the ANG-converting-enzyme inhibitor, captopril, responses to ANG I were reduced. The converting-enzyme inhibitor enhanced pressor responses to ANG II and III but did not alter responses to norepinephrine, U-46619, or serotonin. Moreover, under elevated-tone conditions, pulmonary vasodilator responses to bradykinin were increased following administration of captopril, whereas vasodilator responses to acetylcholine and nitrovasodilators were not altered. These results demonstrate that ANG I, II, and III have similar pulmonary pressor activity and that responses are mediated by ANG II type 1 receptors. Pressor responses to ANG I are reduced, whereas vasodilator responses to bradykinin are enhanced by captopril.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of [Sar1, Ala8]-angiotensin II and hypophysectomy on the intestinal resistance vessels and blood pressure following furosemide-induced volume depletion

1976 ◽  
Vol 54 (3) ◽  
pp. 373-380 ◽  
Author(s):  
J. Robert McNeill ◽  
William C. Wilcox ◽  
Raoul Regnault
Keyword(s):  
Blood Pressure ◽  
Control System ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Adrenal Glands ◽  
The Other ◽  
Volume Depletion ◽  
Competitive Antagonist ◽  
Vasoconstrictor Response ◽  
Resistance Vessels

Intravenous administration of furosemide (2 mg/kg) caused intestinal vasoconstriction in various groups of pentobarbital-anesthetized cats. [Sar1, Ala8]-angiotensin II, a specific competitive antagonist of angiotensin II, was infused 60 min after administration of furosemide, a time when the intestinal vasoconstrictor response to the diuretic was maximal or near maximal. In hypophysectomized animals, infusion of the antagonist abolished the intestinal vasoconstriction and caused a significant fall in arterial pressure even when the intestinal nerves and adrenal glands remained intact. In contrast, the antagonist had little effect when the pituitary gland remained intact. The results suggest that endogenous angiotensin and vasopressin are overlapping mechanisms which constrict the intestinal resistance vessels and support arterial pressure following furosemide-induced volume depletion. In the absence of one control system, the other compensates to maintain the responses.

Haemodynamics of Orally-Active Converting Enzyme Inhibitor (SQ 14225) in Hypertensive Patients

1978 ◽  
Vol 55 (5) ◽  
pp. 453-459 ◽  
Author(s):  
R. J. Cody ◽  
R. C. Tarazi ◽  
E. L. Bravo ◽  
F. M. Fouad
Keyword(s):  
Cardiac Index ◽  
Arterial Pressure ◽  
Enzyme Inhibitor ◽  
Sodium Intake ◽  
Peripheral Resistance ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Resistance Reduction ◽  
Head Up Tilt ◽  
Orally Active

1. The haemodynamic effects of oral converting enzyme inhibitor (SQ 14225) were assessed in eight patients with severe essential or renovascular hypertension. 2. Mean arterial pressure fell (149 ± 5 to 127 ± 8 mmHg, P < 0.02), because of a fall in total peripheral resistance (6.9 ± 0.53 to 5.7 ± 0.40 kPa 1-1 s m2) without a significant change in cardiac index. Two of the eight patients were non-responders without pressure reduction or a haemodynamic change. Sodium restriction (10 mmol/day) while the same dose of SQ 14225 was continued further lowered arterial pressure (137 ± 8 to 111 ± 12 mmHg, P < 0.05) through further resistance reduction (6.5 ± 0.53 to 5.2 ± 0.40 kPa l−1 sm2, P < 0.05). 3. Haemodynamic responses to head-up tilt (increased heart rate and resistance, decreased cardiac index) were unaffected by SQ 14225 regardless of sodium intake. 4. The pattern of reduction in peripheral resistance, with unchanged cardiac index, was similar to that produced by vasodilators acting at both arteriolar and venular levels.

Effects of arterial pressure on drinking and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 264 (1) ◽  
pp. R211-R217 ◽  
Author(s):  
R. L. Thunhorst ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Enzyme Inhibitor ◽  
Urine Volume ◽  
Fluid Retention ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Electrolyte Excretion ◽  
Vasodilator Drug

These experiments examined the dipsogenic responses of rats to intracerebroventricularly administered angiotensin II (ANG II) under normotensive and hypotensive conditions. Intravenous infusion of the vasodilator drug minoxidil (25 micrograms.kg-1.min-1), combined with the angiotensin converting enzyme inhibitor captopril (0.33 mg/min), both reduced blood pressure and prevented endogenous ANG II formation. Central infusions with ANG II (4 or 16 ng/h) began 60 min later, and the intravenous and intracerebroventricular infusions ran concurrently for another 90 min. Mean arterial pressure (MAP), water intake, urine volume (UV) and electrolyte excretion were measured throughout. Water intakes to both doses of intracerebroventricular ANG II were increased, and UV and electrolyte excretion were reduced during hypotensive conditions compared with normotensive conditions. Thus the increased water intakes occurred despite increased fluid retention. It is concluded that arterial hypotension enhances the dipsogenic effects of centrally administered ANG II, possibly through baroreceptor-mediated mechanisms.

Blood pressure maintenance in awake dehydrated rats: renin, vasopressin, and sympathetic activity

1983 ◽  
Vol 245 (2) ◽  
pp. H203-H209 ◽  
Author(s):  
M. Burnier ◽  
J. Biollaz ◽  
D. B. Brunner ◽  
H. R. Brunner
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Sympathetic Activity ◽  
Enzyme Inhibitor ◽  
Inverse Correlation ◽  
Mean Blood Pressure ◽  
Plasma Norepinephrine ◽  
Acute Administration ◽  
Converting Enzyme ◽  
Plasma Arginine

The role of vasopressin, the renin system, and sympathetic activity in sustaining blood pressure in the dehydrated state was investigated in normotensive nonanesthetized male Wistar rats. After 48-h dehydration, plasma arginine vasopressin was 14.0 +/- 1.7 pg/ml and plasma norepinephrine 0.46 +/- 0.05 ng/ml. In another group of rats in which the angiotensin converting enzyme inhibitor (MK 421, 5 mg po twice daily) was administered throughout the dehydration period, blood pressure was reduced by more than 20% (P less than 0.001), and both plasma arginine vasopressin and norepinephrine were higher at 23.4 +/- 3.9 pg/ml (P less than 0.01) and 0.83 +/- 0.07 ng/ml (P less than 0.01), respectively. Taken together, in rats with or without converting enzyme blockade, there was an inverse correlation between mean blood pressure and plasma arginine vasopressin (r = 0.67, P less than 0.01) as well as plasma norepinephrine (r = 0.82, P less than 0.01) levels. The acute administration of a specific vasopressin pressor inhibitor (dPVDAVP) reduced mean blood pressure in the rats with a blocked renin system by 16.9 mmHg (P less than 0.001). In rats without converting enzyme inhibition, the induced fall was only 6.4 mmHg. These results indicate that following 48-h dehydration the renin angiotensin system interacts with the vasopressin secretory mechanism to sustain blood pressure, with renin playing a predominant role. They further suggest that, following blockade of the renin system, activation of the sympathetic nervous system probably also contributes to blood pressure maintenance.

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