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Query: UMLS:C0406810 (
NAME
)
13,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
1. Measurements of changes in renal, mesenteric and hindquarters haemodynamics or cardiac haemodynamics in response to i.v. bolus doses of
arginine vasopressin
(
AVP
) or lysine vasopressin (LVP, 0.7 and 7.0 pmol) were made in conscious, chronically-instrumented Long Evans rats. 2. In some experiments
AVP
and LVP were administered during an infusion of NG-nitro-L-arginine methyl ester (L-
NAME
; 1.0 or 0.3 mg kg-1 h-1) to determine whether or not inhibition of nitric oxide production influenced the cardiovascular effects of the peptides. In other experiments, indomethacin (bolus dose of 5 mg kg-1 followed by infusion at 5 mg kg-1 h-1) was given to determine the possible involvement of cyclo-oxygenase products in the responses to
AVP
and LVP. 3. Under control conditions, the lower dose of LVP had significantly greater effects than
AVP
on heart rate, mean arterial blood pressure, renal, mesenteric and hindquarters conductances, total peripheral conductance, cardiac index, peak aortic flow and +dF/dtmax. The higher dose of LVP had significantly greater effects than
AVP
on all variables (i.e. including stroke index and central venous pressure). 4. In the presence of L-
NAME
(1 mg kg-1 h-1) there was a sustained increase in mean arterial blood pressure (+23 +/- 3 mmHg) and reductions in mesenteric (-38 +/- 4%) and hindquarters (-30 +/- 6%) vascular conductances. Under these conditions the difference in the pressor effects of
AVP
and LVP was abolished, but their differential effects on regional and cardiac haemodynamics persisted. This dose of L-
NAME
did not change cardiac baroreflex sensitivity. 5. During infusion of L-
NAME
at a lower rate (0.3mgkg-th-1), baseline cardiovascular status was unchanged and regional haemodynamic effects of
AVP
and LVP were enhanced, but the differences in the regional vasoconstrictor responses to the two peptides persisted. 6. Indomethacin (5 mg kg-1 bolus, then 5 mg kg- 'h-1 infusion) augmented the renal vasoconstrictor responses to
AVP
and LVP, but abolished the difference in the hindquarters vasoconstrictor responses to the two peptides. However, the differences in the pressor and the renal and mesenteric vasoconstrictor effects of
AVP
and LVP still occurred in the presence of indomethacin. 7. The results indicate that
AVP
normally has lesser cardiovascular effects than LVP but this difference does not seem to be due to more effective stimulation of nitric oxide-mediated or cyclo-oxygenase-dependent vasodilator mechanisms by
AVP
than LVP.
...
PMID:Effects of NG-nitro-L-arginine methyl ester or indomethacin on differential regional and cardiac haemodynamic actions of arginine vasopressin and lysine vasopressin in conscious rats. 204 32
The sensitivity of rat cremaster muscle arterioles to topically applied
arginine vasopressin
(
AVP
) is greatly increased by endotoxin (ENDT) [1]. The hypothesis is that the increase in vasoconstrictor sensitivity is in part due to modification of the
AVP
responses by endothelial compounds such as nitric oxide (NO) and endothelin. Reactivity of left cremaster muscle microvessels of pentobarbital anesthetized Sprague-Dawley rats was measured using videomicroscopy. Femoral arterial pressure as well as second and third order arteriolar (A2 and A3) vasoconstrictor threshold responses were determined for topical
AVP
(10(-15)-10(-6) M). These measurements were repeated in the presence of ENDT (6 mg/kg) alone and in the presence of the NO synthase inhibitor L-
NAME
(N omega-nitro-L-arginine methyl ester; 1 mg/kg) and ENDT (group 1). The control threshold (M)(-log) for arteriolar constriction by
AVP
was 9.4 +/- 0.7. After ENDT the threshold decreased significantly (P < 0.05) to 13.8 +/- 0.5, but returned to 9.0 +/- 0.5 after i.v. injected L-
NAME
. Acetylcholine (ACh) injected i.a. during
AVP
constriction significantly increased diameters at control and after ENDT, but not after L-
NAME
. In group 2 the
AVP
threshold was determined at control, after L-
NAME
plus hydroquinone (HQ), and at 30, 90, and 120 min post-ENDT in the presence of L-
NAME
+ HQ. The
AVP
threshold at control was 9.0 +/- 0.3, after L-
NAME
9.0 +/- 0.6, and after HQ 8.0 +/- 0.7. After L-
NAME
+ HQ, the threshold was significantly increased to 7.3 +/- 0.2. After ENDT, in the presence of both antagonists, the threshold remained elevated at 7.4 +/- 0.2.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Modification of vasopressin microvascular responses by endotoxin, endothelin, and nitric oxide. 751 25
The vasoconstrictor vasopressin has been reported to induce paradoxical local vasodilation in the basilar vasculature through stimulation of the endothelium-derived relaxing factor nitric oxide (NO). We investigated the possibility that at subpressor doses, exogenous
arginine vasopressin
(
AVP
) might have a similar effect in the kidney. Ten Inactin-anesthetized rats were infused with sequential doses of
AVP
from 25 to 6,400 microU/min in 30-min increments. Subpressor infusion resulted in progressive renal vasodilation; renal blood flow (RBF) increased significantly going from 14 +/- 6% above basal at 200 microU/min (p < 0.02) to 27 +/- 5% (p < 0.01) at 1,600 microU/min accompanied by a 24 +/- 5% decrease in renal vascular resistance (RVR). At 6,400 microU/min, blood pressure (BP) increased 29 +/- 6 mm Hg and RVR increased. A second group of 8 rats were first given 10 mg/kg b.w. of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-
NAME
) before infusion of
AVP
. L-
NAME
increased BP 22 +/- 3 mm Hg (p < 0.001), and decreased RBF 16 +/- 3% (p < 0.005). After L-
NAME
, no dose of
AVP
had any further effect on either BP, RBF, or RVR. Continuous infusion of a single subpressor dose of 100 microU
AVP
resulted in a 26% increase in RBF (from 7.52 +/- 0.68 to 9.49 +/- 0.54 ml/min/g kidney weight, p < 0.001).
AVP
doubled urinary cyclic guanosine monophosphate excretion, a marker for renal NO synthesis, from 8.51 +/- 1.01 to 17.48 +/- 4.26 pM/min (p < 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Arginine vasopressin-induced renal vasodilation mediated by nitric oxide. 773 55
1. The effects of vasopressin and deamino-8-D-
arginine vasopressin
(DDAVP, desmopressin) were studied in artery rings (0.8-1 mm in external diameter) obtained from portions of human omentum during the course of abdominal operations (27 patients). 2. In arterial rings under resting tension, vasopressin produced concentration-dependent, endothelium-independent contractions with an EC50 of 0.59 +/- 0.12 nM. The V1 antagonist d(CH2)5Tyr(Me)AVP (1 microM) and the mixed V1-V2 antagonist desGly-d(CH2)5D-Tyr(Et)ValAVP (0.01 microM) displaced the control curve to vasopressin to the right in a parallel manner without differences in the maximal responses. In the presence of indomethacin (1 microM) the contractile response to vasopressin was significantly increased (P < 0.01). 3. In precontracted arterial rings, previously treated with the V1 antagonist, d(CH2)5Tyr(Me)AVP (1 microM), vasopressin produced endothelium-dependent relaxation. This relaxation was reduced significantly (P < 0.05) by indomethacin (1 microM) and unaffected by the V1-V2 receptor antagonist desGly-d(CH2)5D-Tyr(Et)ValAVP (1 microM) or by NG-nitro-L-arginine methyl ester (L-
NAME
, 0.1 mM). 4. The selective V2 receptor agonist, DDAVP, caused endothelium-independent, concentration-dependent relaxations in precontracted arterial rings that were inhibited by the mixed V1-V2 receptor antagonist, but not by the V1 receptor antagonist or by pretreatment with indomethacin or L-
NAME
. 5. Results from this study suggest that vasopressin is primarily a constrictor of human mesenteric arteries by V1 receptor stimulation; vasopressin causes dilatation only during V1 receptor blockade. The relaxation appears to be mediated by the release of vasodilator prostaglandins from the endothelial cell layer and is independent of V2 receptor stimulation or release of nitric oxide. In contrast, the relaxation induced by DDAVP is largely dependent on stimulation of V2 receptors.
...
PMID:Relaxation of human isolated mesenteric arteries by vasopressin and desmopressin. 783 91
The roles of the sympathetic nervous system, angiotensin II, and
arginine vasopressin
in the cardiovascular-renal responses to nitric oxide synthesis inhibition were examined in eight conscious dogs equipped with arterial and venous catheters and a nonoccluding bladder catheter. Nitric oxide inhibition was achieved by intravenous infusion of NG-nitro-L-arginine methyl ester (L-
NAME
) at 37.1 nmol/kg per minute for 140 minutes in the control group. The same dogs, after a 1-week recovery, were pretreated for 2 days with either prazosin for alpha 1 blockade, prazosin plus propranolol for alpha 1 plus beta blockade, L-158,809 for angiotensin receptor blockade, or d(CH2)Tyr(Me)
arginine vasopressin
for vasopressin-V1 blockade, and the L-
NAME
infusion was repeated. After 140 minutes of L-
NAME
infusion into the control group, mean arterial pressure and renal vascular resistance had increased 16% and 71%, and renal blood flow, glomerular filtration rate, urine flow, and urinary sodium excretion had decreased 33%, 16%, 61%, and 64%, respectively. The decrement in renal blood flow and glomerular filtration during L-
NAME
administration was unaffected by any of the neurohumoral blockers. During V1 blockade L-
NAME
resulted in only a 3% increase in arterial pressure, attenuation of the renal vascular resistance response, and almost total elimination of the decrease in urine flow. During angiotensin blockade the L-
NAME
-induced increase in arterial pressure was markedly attenuated, and the decrease in urinary sodium excretion was attenuated in the alpha 1 plus beta blockade group.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Mechanisms involved in the cardiovascular-renal actions of nitric oxide inhibition. 820 34
Renal vasoconstrictor responses to the adenosine A1 agonist N6-cyclopentyladenosine (CPA) were compared in the in situ autoperfused rat kidney to responses evoked by angiotensin II (ANG II), endothelin-1 (ET-1),
arginine vasopressin
(
AVP
), carbocyclic thromboxane A2 (CTxA2), phenylephrine (PE), and 5-hydroxytryptamine (5-HT). On the basis of their ED50 values (dose of agonist, in mass units, that produced 50% of maximal response to that agonist), the order of vasoconstrictor potency was ANG II > or =
AVP
> ET-1 > CPA > 5-HT > or = PE > CTxA2. Dose-response curves to CPA were shallower and maximal responses were weaker than those produced by the other agonists. Maximal responses, the log ED50, and the slope of the dose-response curve to CPA were markedly potentiated in the presence of the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester (L-
NAME
). Selective antagonism of A1 receptors increased renal blood flow and markedly attenuated CPA-induced renal vasoconstriction in the absence or presence of L-
NAME
but had no effect on the maximal responses to ANG II. Conversely, AT1 receptor antagonism attenuated renal vasoconstriction produced by ANG II but had little effect on the produced by CPA. These results suggest that endogenous NO modulates renal vasoconstriction produced by A1 receptor stimulation and provide evidence against an interaction between renovascular adenosine A1 and angiotensin AT1 receptors.
...
PMID:Interactions of adenosine A1 receptor-mediated renal vasoconstriction with endogenous nitric oxide and ANG II. 823 45
Experiments were performed in conscious chronically instrumented dogs to study the mechanism of hemodynamic effects mediated by selective vasopressin V2 agonists. In one group of dogs (n = 5) instrumented for the measurement of arterial pressure and cardiac output (electromagnetic flowmeter), the infusion of NG-nitro-L-arginine methyl ester (L-
NAME
; 20 or 40 micrograms.kg-1 x min-1) prevented or significantly inhibited the increase in cardiac output, heart rate and systemic conductance induced by injections of 1-desamino-8-D-
arginine vasopressin
(DDAVP, desmopressin) and 4-valine-8-D-
arginine vasopressin
(VDAVP), two selective V2 agonists. L-
NAME
infusion did not modify the aortic adenosine 3',5'-cyclic monophosphate increase induced by DDAVP infusion. In a second group of dogs similarly prepared (n = 4), the administration of L-arginine (10 mg.kg-1 x min-1) at the same time as that of L-
NAME
(20 micrograms.kg-1 x min-1) completely prevented the hemodynamic effects of L-
NAME
and restored the response to DDAVP administration. In a third group of dogs (n = 4), the infusion of a bradykinin B2 antagonist, at a rate that significantly inhibited the cardiac output, heart rate, and blood pressure responses to bradykinin, did not modify the hemodynamic response to DDAVP infusion. We conclude that the hemodynamic effects of selective V2 agonists in dogs are not mediated by bradykinin release but instead via a V2-like receptor on endothelial cells that triggers the release of nitric oxide.
...
PMID:L-NAME antagonizes vasopressin V2-induced vasodilatation in dogs. 830 28
In a comparison of the spontaneously hypertensive rat (SHR) with Wistar-Kyoto (WKY) and Sprague Dawley (SD) rats, it was shown that pertussis toxin (PTX) lowers the blood pressure of the SH but not WKY or SD rats. Sympathetic nerve stimulation (SNS), via the pithing rod, the nitric oxide NO)-synthase inhibitor NW-Nitro-L-arginine methyl ester L-
NAME
) and the pressor response to infusion of
AVP
were also observed. The results indicate that a G-protein(s) population and/or function may be altered in the vascular smooth muscle of SH rats. This dysfunction may contribute to the heightened pressor responsiveness of the SHR vasculature to SNS and
arginine vasopressin
(
AVP
) and the increased sensitivity to the hypotensive effects of nifedipine. NO-synthase activity also appears to be increased in the SHR, suggesting that this increase should reflect a compensatory change due to the elevation of BP in SHR.
...
PMID:Changes in vascular smooth muscle function in hypertension. 832 52
It has become evident that complete elimination of the vasodilator response to agonists that require the release of nitric oxide (NO) is necessary for certain studies of the microcirculation. The A2 and A3 arterioles of the rat cremaster muscle microcirculation were studied by video-microscopy. At control, arterioles at rest or constricted by
arginine vasopressin
(
AVP
) were dilated by intra-arterially injected acetylcholine (ACh), intra-arterially injected adenosine (ADO) and topical adenosine. The NO antagonists, Nw-nitro-L-arginine methyl ester (L-
NAME
) and hydroquinone (HQ), which acts as an antagonist by generating free radicals, in maximal doses, individually partially blocked the vasodilator actions of intra-arterial ACh and intra-arterial ADO. Combining L-
NAME
and HQ eliminated the vasodilation by intra-arterial ACh and intra-arterial ADO. Sodium nitroprusside dilated the arterioles to the resting level or above at control and in the presence of the antagonists either individually or when combined. However, the NO antagonists did not block the arteriolar vasodilator responses to topical ADO. The reduction of the production of NO and enhancement of its destruction by superoxide radicals results in the total absence of the vasodilator response due to intra-arterially injected acetylcholine and adenosine. The data suggest that luminal ADO receptors cause arteriolar dilation by endothelial-dependent mechanisms and abluminal receptors cause dilation by another mechanism.
...
PMID:Antagonism of acetylcholine and adenosine rat cremaster arteriolar vasodilation by combination of NO antagonists. 837 62
Endothelium-dependent relaxation of mesenteric resistance arteries of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats was studied. Acetylcholine-induced relaxation of SHR vessels precontracted with 10 microM norepinephrine was endothelium dependent and attenuated compared with WKY vessels. The impaired response of SHR vessels was normalized by inhibition of cyclooxygenase with indomethacin. Blockade of nitric oxide synthetase with NG-nitro L-arginine methyl ester (L-
NAME
) or inhibition of guanylate cyclase with methylene blue attenuated acetylcholine-induced relaxation of norepinephrine-contracted SHR vessels but had no effect on WKY vessels. When vessels were precontracted with 30 nM
arginine vasopressin
, acetylcholine induced similar degrees of relaxation in both strains. A similar response was detected when lysine vasopressin was used to induce tone. Indomethacin had no effect on relaxation responses of SHR and WKY vessels precontracted with either form of vasopressin. L-
NAME
and methylene blue partially inhibited acetylcholine-induced relaxation of vasopressin-contracted vessels from both strains. Acetylcholine added at baseline did not induce contraction of vessels from either strain. It is concluded that endothelium-dependent relaxation of SHR resistance arteries is not impaired under all circumstances. Acetylcholine-induced relaxation may be suppressed in SHR resistance arteries when norepinephrine is used to induce contraction as a result of catecholamine-induced production of an endothelium-derived contracting factor. Vasopressin, on the other hand, does not elicit production of this contracting factor and may enhance the vasorelaxant action of acetylcholine in resistance arteries of both strains via actions on endothelial or vascular smooth muscle cells.
...
PMID:Endothelium-dependent relaxation of hypertensive resistance arteries is not impaired under all conditions. 841 84
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