Systemic and regional hemodynamic effects of endogenous vasopressin stimulation in rats

Charocopos, Fotis; Hatzinikolaou, Peter; North, William G.; Gavras, H

doi:10.1152/ajpheart.1982.243.4.h560

Cited by 10 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…17 Endothelium-derived nitric oxide is the final mediator of many vasodilator substances, as mentioned above. However, different vascular trees may display different sensitivity to the action of a given vasoactive substance, as has been shown in the past for angiotensin, 26 bradykinin, 21 vasopressin, 27 and others.…”

Section: Effects Of N G -Monomethyl L-arginine On Systemic and Regionmentioning

confidence: 93%

Inhibition of nitric oxide, bradykinin, and prostaglandins in normal rats.

Wang¹,

Gavras²,

Wierzba³

et al. 1992

Hypertension

View full text Add to dashboard Cite

We assessed the vasodilator effect of endothelium-derived nitric oxide by inhibiting its formation with JV G -monomethyl L-arginine (LNMMA) on systemic and regional hemodynamics in conscious, normotensive rats, using the radioactive microsphere technique. In rats injected with 10 mg/kg LNMMA (n=8), mean blood pressure increased by 16.2±2.6 mm Hg, and heart rate decreased by 543 ±16.7 beats per minute. In comparison with rats injected with 5% dextrose (n=14), cardiac index was lower by 35.6% (/?<0.01), and total peripheral vascular resistance was higher by 51.6% (p<0.01); regional blood flows were lower and vascular resistance higher in most organs. Changes were significant in the heart, kidney, stomach, large intestine, skin, and adrenals (/?<0.05). Preinjection of 100 mg/kg L-arginine prevented the pressor response but only partially attenuated the other hemodynamic effects of LNMMA. Combination of LNMMA with the bradykinin antagonist (D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg)trifluoroacetic acid (50 jtg/min for 5 minutes) did not produce systemic or regional effects different from those obtained with LNMMA alone. Combination of LNMMA with indomethacin (10 mg/kg) resulted in additional changes in the cerebral circulation, blood flow decreasing by an additional 44.2% (p<0.01) and vascular resistance increasing by 753% (p<0.01) compared with changes produced by LNMMA alone. The data suggest that endothelium-derived nitric oxide contributes differently to the resting vascular tone of various vascular beds; it mediates most of the vasodilator effects of bradykinin and partly those of prostaglandins, but the effect of the latter on the cerebral circulation is not nitric oxide dependent (Hypertension 1992;19 [suppl II]:II-255-II-261)E ndothelium-derived relaxing factor (EDRF) is a vasodilator substance generated by endothelial cells within the vessel wall. Many vasodilators, such as bradykinin, acetylcholine, and substance P, induce relaxation of isolated vascular tissue by release of EDRF 12 and therefore are called endothelium-dependent vasodilators. Recent evidence indicates that the main EDRF is nitric oxide 3 -11 and that its biosynthetic precursor is L-arginine. 1012 Af G -Monomethyl L-arginine (LNMMA) was found to inhibit vascular nitric oxide production in endothelial cells and thus inhibit relaxation induced by endothelium-dependent vasodilators both in vitro 12 -13 and in vivo. 1415 Inhibition of the endotheliumderived nitric oxide formation by LNMMA increased blood pressure in anesthetized rabbits, 14 rats, 15 and guinea pigs 16 and decreased forearm blood flow in

show abstract

Section: Effects Of N G -Monomethyl L-arginine On Systemic and Regionmentioning

confidence: 93%

Inhibition of nitric oxide, bradykinin, and prostaglandins in normal rats.

Wang¹,

Gavras²,

Wierzba³

et al. 1992

Hypertension

View full text Add to dashboard Cite

show abstract

“…AVP caused a direct coronary constriction and negative inotropism in dogs, 30 " 32 whereas it had no effects on coronary flow and resistance in rats, 20 -33 despite causing a declined cardiac performance. 20 The decrease in resistance, but not increase in flow, seen in the spleen following AVP blockade in whole and responder DOCA-salt rats (Figure 4) outweighed in a relative magnitude those seen in DOCA-salt rats that received no AVP antagonist (Experiment 3A). Accordingly, AVP may contribute in some way to elevated splenic resistance in these rats.…”

Section: (Ks3mentioning

confidence: 89%

“…20 " 22 24 One of the analogs acts as a partial agonist in dogs, but not in rats. 17 No such observations were made with the antagonist that we and other investigators used.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular hemodynamics and vasopressin blockade in DOCA-salt hypertensive rats.

Yamamoto¹,

Yamane²,

Umeda³

et al. 1984

Hypertension

View full text Add to dashboard Cite

SUMMARY In conscious rats with near-malignant phases of DOCA-salt (DS) hypertension, hemodynamics were studied with microspheres before and after administration of a vasopressin (VP) vasopressor antagonist in relation to plasma VP levels (pVP). Compared to the controls, the DS rats showed significant elevations in mean arterial pressure (MAP), total vascular resistance (TVR), and pVP, and a flow redistribution from kidney and spleen to skeletal muscles and heart, with increased vascular resistance in almost all organs. The antagonist elicited no significant systemic hemodynamic effects in DS rats as a whole; however, two subgroups, responders vs nonresponders, were identified according to the effects on MAP. In responders with a pVP of 29.2 ± 2.7 (SE) pg/ml, the antagonist lowered MAP (-24.9 ± 5.9 mm Hg) and TVR significantly, while in nonresponders with a pVP of 15.2 ± 3.4 pg/ml, there were no effects. The major antagonist-induced regional responses were increased flow and decreased vascular resistance in skeletal muscles and skin in whole DS rats, and additionally in the gastrointestinal tract, portal organs, and testes in the responders. Significant correlations were observed between pVP, MAP, TVR,and depressor responses to the antagonist only when all data for DS and control rats were pooled. Thus, the systemic hemodynamic effects of VP are important only in responders with exceedingly elevated pVP. VP contributes significantly to the regional hemodynamic abnormalities in skeletal muscles and skin in whole DS rats, and also in several other organs in the responders. (Hypertension 6: 397-407, 1984) KEY WORDS * systemic and regional hemodynamics vasopressin vasopressor antagonist plasma vasopressin level A RGININE vasopressin (AVP) has been implicated in the pathogenesis of deoxycorticosterone (DOCA)-salt hypertension in the rat. Supporting evidence includes: 1) increased plasma concentrations 1 " 3 and urinary excretions 6 of AVP; 2) an acute, substantial fall in blood pressure after administration of either specific AVP antisera 1 -3 or specific antagonists 6 of the vasopressor action of AVP; and 3) the necessity of AVP replacement for the production of DOCA-salt hypertension in hypothalamic diabetes insipidus rats lacking AVP.3 -6 " 9 AVP effects may involve antidiuretic activity 9 and other mechanisms, 8 but the influence of AVP on the vascular system is considered to be an important factor, since the blood pressure was lowered before or without induction of diuresis when AVP antisera or AVP vasopressor antagonists were used. However, Bumier et al. 10 noted that there was no decrease in blood pressure following administration of an antagonist in DOCA-salt hypertensive rats and no elevated plasma AVP after 4 weeks of treatment. Rabito et al." and Rascher et al. 12 experienced similar failures with antagonists in rats with malignant hypertension (plasma AVP level not given), and in rats with established hypertension and concomitantly elevated plasma AVP levels. Controversy thus exists as to the effectiv...

show abstract

“…3 Differences between diabetics treated with dobutamine (group III) and those treated with MK-422 (group IV). Cardiac output and regional blood flows were de termined by a modification of the radioactive micro sphere method [3] as described elsewhere [4], In brief, approximately 50,000 radioactive microspheres (NEN-TRAC), 15 ± 3 pm in diameter and labelled with ll3Sn at a specific activity of 10 mCi/g, were sus pended in a sucrose solution with a specific gravity close to that of the microspheres (i.e., 1.3 g/ml) with 1 drop of Tween 80 added to the suspension. After ultra sonic and mechanical agitation for 20 min and micro scopic observation for adequate mixing, 0.10 ml of the solution was injected over 20 s, through an airtight syringe (Hamilton.…”

Section: Methodsmentioning

confidence: 99%

Cardiovascular Effects of Dobutamine and Converting Enzyme Inhibition in Rats with Diabetic Ketoacidosis

Charocopos

Gavras

1985

Pharmacology

View full text Add to dashboard Cite

We investigated cardiac and peripheral hemodynamics in rats with streptozotocin-induced diabetes mellitus in comparison to normal controls. Diabetic rats showed a significantly decreased cardiac output and heart rate, with unchanged mean blood pressures. Regional blood flows were unchanged except for renal blood flow which was significantly lower. The low output state associated with diabetes was reversed by angiotensin converting enzyme inhibition with MK-422, but not with dobutamine, although both agents caused similar reduction in peripheral vascular resistance. However, despite improved left ventricular performance, renal perfusion did not improve after MK-422.

show abstract

Systemic and regional hemodynamic effects of endogenous vasopressin stimulation in rats

Cited by 10 publications

References 0 publications

Inhibition of nitric oxide, bradykinin, and prostaglandins in normal rats.

Inhibition of nitric oxide, bradykinin, and prostaglandins in normal rats.

Cardiovascular hemodynamics and vasopressin blockade in DOCA-salt hypertensive rats.

Cardiovascular Effects of Dobutamine and Converting Enzyme Inhibition in Rats with Diabetic Ketoacidosis

Contact Info

Product

Resources

About