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Query: UMLS:C0406810 (
NAME
)
13,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Endothelium-derived relaxing factor has been shown to regulate renal blood flow, and inhibition of its synthesis increases blood pressure and renal vascular resistance and decreases renal blood flow. Using the substrate antagonist NW-nitro-L-arginine methyl ester (L-
NAME
), we tested whether renal vasoconstriction induced by endothelium-derived relaxing factor synthesis inhibition could be mediated in part by angiotensin II. In 14 control rats, 10 mg/kg body wt L-
NAME
increased blood pressure from 106 +/- 6 to 126 +/- 6 mm Hg (p < 0.001), increased renal vascular resistance by 74% (from 19.3 +/- 2.6 to 33.6 +/- 2.9 resistance units), and decreased renal blood flow by 34% (from 5.9 +/- 0.5 to 3.9 +/- 0.3 ml.min-1.g kidney wt-1, p < 0.005). When six rats were treated with 10 mg/kg body wt of the
angiotensin receptor
antagonist DuP 753, L-
NAME
increased blood pressure from 84 +/- 4 to 106 +/- 4 mm Hg (p < 0.001); however, renal vascular resistance increased by only 27% (from 13 +/- 2 to 17 +/- 3 resistance units, p < 0.01; p < 0.05 different from control value) and renal blood flow was unchanged. Likewise, after pretreatment of six rats with 32 micrograms/100 g body wt of the angiotensin converting enzyme inhibitor enalaprilat, L-
NAME
increased blood pressure from 88 +/- 5 to 124 +/- 6 mm Hg (p < 0.001) and renal vascular resistance by 54% (from 12 +/- 1 to 18 +/- 3 resistance units, p < 0.01; p < 0.05 different from control value) but renal blood flow was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Angiotensin dependence of endothelium-mediated renal hemodynamics. 133 Sep 22
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
We investigated whether chronic deficiency of nitric oxide (NO) in stroke-prone spontaneously hypertensive rats (SHRSP) precipitates stroke and whether exogenous nitrates and other pharmacological agents can prevent stroke. Groups of five-week-old male SHRSP rats chronically received saline, L-nitro-arginine methyl ester (L-NAME) in saline, L-
NAME
along with pharmacological agents (L-arginine, isosorbide dinitrate, enalapril maleate and L-158,809;
angiotensin receptor
antagonist; 5,7-dimethyl-2-ethyl-3(-)[[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]meth yl]-imidazo[4,5-b]pyridine) in saline to drink. The development of visible neurological deficits following various treatments was considered as an occurrence of stroke. Within hours following onset of stroke, the rats were anesthetized, catheterized and attached to a Cardiomax blood pressure recorder. SHRSP treated with L-
NAME
(10+/-2 mg/day) developed stroke in 11+/-2 days while no neurological deficit was seen in animals receiving saline till the end of the study period (35 days). Blockade of the renin-angiotensin system with enalapril or L-158,809 significantly delayed the onset of stroke (19+/-2 and 20+/-2 days, respectively), but caused only slight reductions in mean arterial blood pressure. These results suggest that chronic inhibition of NO synthase in SHRSP is associated with the development of stroke and such stroke appears to be renin-angiotensin system-dependent.
...
PMID:Angiotensin receptor antagonists delay nitric oxide-deficient stroke in stroke-prone rats. 931 59
We measured the activity of mitogen-activated protein (MAP) kinases, enzymes believed to be involved in the pathway for cell proliferation, in rat aortic strips with or without endothelium, and examined effects of
angiotensin receptor
antagonists, endothelin receptor antagonists and nitric oxide (NO)-related agents. Endothelium removal produced an activation of MAP kinase activity in the strips, whereas the enzyme activity was not affected in the adventitia. The MAP kinase activation was inhibited by either the angiotensin AT1 receptor antagonist losartan or the endothelin ETA receptor antagonist BQ 123. The combination of both antagonists caused an additive inhibition. The angiotensin AT2 receptor antagonist PD 123,319 and the endothelin ETB receptor antagonist BQ 788 did not affect the MAP kinase activation. The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-
NAME
) caused an activation of MAP kinase in the endothelium-intact aorta and the MAP kinase activation was inhibited by losartan or BQ123. The NO releaser nitroprusside inhibited the MAP kinase activation induced by endothelium removal or angiotensin II. These results suggest that even in isolated arteries, NO of endothelial origin tonically exert MAP kinase-inhibiting effects and endogenous angiotensin II and endothelins in the media are tonically released to cause MAP kinase-stimulating effects in medial smooth muscle.
...
PMID:Evidence that angiotensin II, endothelins and nitric oxide regulate mitogen-activated protein kinase activity in rat aorta. 965 1
This study was designed to investigate the effects of chronic inhibition of NO synthesis as well as chronic
angiotensin receptor
blockade with losartan in the development of hypertension, on mesenteric arterial bed reactivity as well as on the development of cardiac and kidney hypertrophy in deoxycorticosterone-salt (DOCA) hypertension. Uninephrectomized rats were divided in four experimental groups all receiving saline water to drink and treated or not with losartan over a period of 9 days. Two of these groups were administered DOCA, one of which received also N(G)-nitro-L-arginine-methyl ester (L-
NAME
) to drink. A third group received only L-
NAME
, while another group received only saline. Systolic blood pressure was similarly increased in L-
NAME
, DOCA, DOCA-L-
NAME
groups. Cardiac and kidney weights were increased in DOCA but significantly reduced in DOCA-L-
NAME
. Losartan prevented the development of hypertension in all groups and also prevented cardiac and kidney hypertrophy in DOCA. The hyperreactivity of mesenteric arteries to phenylephrine, measured in the presence of indomethacin, was endothelium-dependent in both L-
NAME
groups but not in DOCA rats. Pretreatment with BQ 123 did not modify these endothelium-dependent responses in L-
NAME
rats. Chronic losartan prevented endothelium-dependent phenylephrine hyperreactivity only in DOCA, whereas only the removal of the endothelium attenuated the responsiveness in both L-
NAME
-treated groups. Vasorelaxations to acetylcholine and isoproterenol were attenuated in the three hypertensive groups and were normalized only in DOCA and L-
NAME
treated with losartan. In summary, in all hypertensive groups, blood pressure was normalized by losartan independently of its effects on endothelial functions. In DOCA, losartan normalized the phenylephrine hyperreactivity through an endothelial-dependent mechanism. However, in L-
NAME
-treated groups an endothelial-derived contracting factor, other than angiotensin II, endothelin, or vasoconstrictor prostanoids, appears to be activated. Both NO and angiotensin II seem to play a role in the early development of hypertension and organ hypertrophy in DOCA hypertension.
...
PMID:Role of NO and angiotensin II in the early development of endothelial functions impairment and cardiac hypertrophy in deoxycorticosterone acetate-salt hypertension. 992 5
Footshocks increased mean arterial pressure and heart rate. Systemic administration of losartan, a specific angiotensin AT(1) receptor antagonist, not only inhibited the pressor response to footshocks, but also resulted in vasodepression. Administration of 1-[[4-(dimethylamino)3-methylphenyl]methyl]-5 (diphenylacetyl)-4,5,6, 7-tetrahydro-1H imidazol (4,5-c] pyridine-6-carboxilic acid, ditrifluoro acetatemonohydrate (PD 123319), a specific angiotensin AT(2) receptor antagonist, did not alter the hemodynamic response to footshocks. Simultaneous blockade of angiotensin AT(1) and AT(2) receptors by combined administration of losartan and PD 123319, eliminated the vasodepressor response to footshocks unmasked in losartan-pretreated rats. Saralasin, a non-specific
angiotensin receptor
antagonist, abolished the cardiovascular response to footshocks similarly like the losartan+PD 123319 treatment. Our data suggest that the vasodepressor response to footshocks in the presence of an angiotensin AT(1) receptor antagonist is triggered by activation of angiotensin AT(2) receptors. We studied the role of kinins, nitric oxide and prostaglandins in the vasodepressor response observed after footshocks. The decrease in mean arterial pressure observed after footshocks in losartan-treated rats was blunted by icatibant (HOE 140), N(G)-nitro-L-arginine-methyl ester (L-
NAME
) or indomethacin, indicating that kinins, nitric oxide and prostaglandins appear to be involved in the pressure response to footshocks during angiotensin AT(1) receptor blockade.
...
PMID:Angiotensin AT(2) receptors mediate vasodepressor response to footshock in rats. Role of kinins, nitric oxide and prostaglandins. 1077 Oct 41
Chronic inhibition of NO synthesis induces cardiac hypertrophy independent of systemic blood pressure (SBP) by increasing protein synthesis in vivo. We examined whether ACE inhibitors (ACEIs) enalapril and temocapril and angiotensin II type-I receptor antagonists (
angiotensin receptor
blockers [ARBs]) losartan and CS-866 can block cardiac hypertrophy and whether changes in activation of 70-kDa S6 kinase (p70S6K) or extracellular signal-regulated protein kinase (ERK) are involved. The following 13 groups were studied: untreated Wistar-Kyoto rats and rats treated with NO synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-
NAME
), D-
NAME
(the inactive isomer of L-
NAME
), L-
NAME
plus hydralazine, L-
NAME
plus enalapril (3 mg. kg(-1). d(-1)) or temocapril (1 or 10 mg. kg(-1). d(-1)), L-
NAME
plus losartan (10 mg. kg(-1). d(-1)) or CS-866 (1 or 10 mg. kg(-1). d(-1)), L-
NAME
plus temocapril-CS866 in combination (1 or 10 mg. kg(-1). d(-1)), and L-
NAME
plus rapamycin (0.5 mg. kg(-1). d(-1)). After 8 weeks of each experiment, ratios of coronary wall to lumen (wall/lumen) and left ventricular weight to body weight (LVW/BW) were quantified. L-
NAME
increased SBP, wall/lumen, and LVW/BW compared with that of control. ACEIs, ARBs, and hydralazine equally canceled the increase in SBP induced by L-
NAME
. However, ACEIs and ARBs equally (but not hydralazine) attenuated increase in wall/lumen and LVW/BW induced by L-
NAME
. The L-
NAME
group showed both p70S6K and ERK activation in myocardium (2.2-fold and 1.8-fold versus control, respectively). ACEIs inactivated p70S6K and ARBs inactivated ERK in myocardium, but hydralazine did not change activation of either kinase. Thus, ACEIs and ARBs modulate different intracellular signaling pathways, inhibiting p70S6K or ERK, respectively, to elicit equal reduction of cardiac hypertrophy induced by chronic inhibition of NO synthesis in vivo.
...
PMID:Differential subcellular actions of ACE inhibitors and AT(1) receptor antagonists on cardiac remodeling induced by chronic inhibition of NO synthesis in rats. 1156 13
The effect of angiotensin-(1-7) on jejunal water absorption in rats was investigated. The jejunal sac of anesthetized rats was filled with two ml of tyrode solution containing 3.7 MBq of tritiated water. A femoral vein was cannulated for administration of peptides and drugs. Infusion of Ang-(1-7) at the dose of 0.7 ng/kg.min produced a significant increase in jejunal water absorption compared to control (32% increase). The Ang-(1-7) antagonist A-779 abolished the effect of Ang-(1-7) on water absorption. A reduction of the Ang-(1-7) effect was also produced by treatment with the AT(1) receptor antagonist, losartan or the AT(2) receptor antagonist, PD123.177. The increase in jejunal water absorption produced by Ang-(1-7) was blocked by the nitric oxide synthase inhibitor, L-
NAME
and by indomethacin. These data suggest that the effect of Ang-(1-7) on the jejunal loop is mediated by activation of a multiple angiotensin receptors and/or by an atypical
angiotensin receptor
. Furthermore, the effect of Ang-(1-7) on jejunal water absorption is mediated by nitric oxide and by a cyclooxygenase-dependent mechanism.
...
PMID:Effect of angiotensin-(1-7) on jejunal absorption of water in rats. 1181 17
Although the angiotensin-converting enzyme (ACE) inhibitor-induced bradykinin enhances nitric oxide (NO) release, bradykinin may also stimulate the production of an additional vasodilator, endothelium-derived hyperpolarizing factor (EDHF). This study examined the role of EDHF in mediating the NO-independent action of ACE inhibitors in canine renal microcirculation in vivo. We used intravital CCD camera videomicroscopy that allowed direct visualization of renal microcirculation in superficial and juxtamedullary nephrons in an in vivo, in situ, and relatively intact setting. In the presence of E4177 (an
angiotensin receptor
blocker), cilazaprilat (30 microg/kg) had no effect on diameter of superficial afferent arterioles (Aff), but it increased renal contents of bradykinin and nitrate plus nitrite, and it elicited dilation of juxtamedullary Aff (from 24.0+/-0.2 to 28.2+/-0.8 microm), juxtamedullary efferent arterioles (Eff) (from 24.2+/-0.2 to 28.0+/-0.8 microm), and superficial Eff (from 18.2+/-0.2 to 19.7+/-0.2 microm). These changes in diameters were prevented by N(alpha)-adamantaneacetyl-d-Arg-[Hyp(3),Thi(5,8),D-Phe(7)]bradykinin, a bradykinin receptor antagonist. The pretreatment with nitro-l-arginine methylester (l-
NAME
) plus E4177 eliminated the dilator response of juxtamedullary/superficial Eff and the increase in renal nitrate plus nitrite levels induced by cilazaprilat. In contrast, in the presence of E4177+l-
NAME
, cilazaprilat still caused 8%+/-3% dilation of juxtamedullary Aff, which was completely eliminated by proadifen, a cytochrome-P450 and K(Ca) channel blocker. Collectively, the ACE inhibitor exerts multiple vasodilator mechanisms, including the inhibition of angiotensin II formation; blockade of angiotensin II activity appears to be a dominant mechanism in superficial Aff, whereas the bradykinin-induced NO acts on superficial Eff and juxtamedullary Aff/Eff. Furthermore, a putative EDHF is an additional mechanism for the ACE inhibitor-induced vasodilation of juxtamedullary Aff in vivo.
...
PMID:Role of endothelium-derived hyperpolarizing factor in ACE inhibitor-induced renal vasodilation in vivo. 1475 81
A biphasic cardiovascular response to bolus i.v. injection of human urotensin II (hUII, 3 nmol kg(-1)) in conscious, male, Sprague-Dawley (SD) rats was identified and underlying mechanisms were explored. Initially (0-5 min) there was tachycardia, hypotension and mesenteric and hindquarters vasodilatation; later (30-120 min), tachycardia, hindquarters vasodilatation and a modest rise in blood pressure occurred. Pretreatment with indomethacin or N(G) nitro-l-arginine methylester (l-
NAME
) reduced the mesenteric vasodilator response to hUII, and abolished the late tachycardia and hindquarters vasodilatation. Indomethacin also abolished the hypotension and early hindquarters vasodilatation, and substantially reduced the initial tachycardia. Indomethacin and l-
NAME
together prevented all haemodynamic responses to hUII. Inhibition of inducible NOS had no effect on responses to hUII, whereas inhibition of neuronal NOS reduced the delayed tachycardic response to hUII but did not significantly affect the vasodilatation. Only the initial tachycardic response to hUII was antagonised by propranolol. In spontaneously hypertensive rats (SHR), the initial haemodynamic responses to hUII were qualitatively similar to those in SD rats, although there was also a modest renal vasodilatation. The secondary response comprised a smaller tachycardia and a small rise in blood pressure, with no significant hindquarters vasodilatation. Haemodynamic responses to hUII were not enhanced by endothelin and
angiotensin receptor
antagonism in either SD rats or in SHRs. One interpretation of these results is that the primary response to bolus injection of hUII is prostanoid- or prostanoid- and NO-mediated (mesenteric vasodilatation) and that this triggers secondary events, which are dependent on eNOS (hindquarters vasodilatation) and neuronal NOS (tachycardia).
...
PMID:Bolus injection of human UII in conscious rats evokes a biphasic haemodynamic response. 1533 62
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