Marked Regional Heterogeneity in the Magnitude of EDRF/NO-Mediated Vascular Tone in Awake Rats

Greenblatt, Eric P.; Loeb, Alex L.; Longnecker, David E.

doi:10.1097/00005344-199302000-00008

Cited by 55 publications

(32 citation statements)

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“…As a result of these differential enhancements, the vascular sympathoinhibitory effects of losartan were suppressed by L-NAME (except in the kidney) thus pointing out the major responsibility of NO in their development. This responsibility is furthermore emphasized by our experiments showing that when L-arginine is administered in a dose that counteracts most but not all, a finding previously reported by others (Gardiner et al, 1990;Greenblatt et al, 1993), L-NAME haemodynamic effects, it fully restores the sympathoinhibitory effects of losartan. Finally, in the kidney and in contrast to all other investigated vascular beds, NO appears not to be predominantly involved in the sympathoinhibitory effects of losartan.…”

Section: Discussionsupporting

confidence: 60%

Involvement of nitric oxide, but not prostaglandins, in the vascular sympathoinhibitory effects of losartan in the pithed spontaneously hypertensive rat

Richer

Domergue

Vincent

et al. 1996

British J Pharmacology

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1 The aim of this study was to investigate whether nitric oxide (NO) and/or vasodilator prostaglandins (PGs) are involved in the sympathoinhibitory effects exerted by losartan versus the vascular responses elicited by spinal cord electrical stimulation (SCS) in pithed spontaneously hypertensive rats (SHRs).2 SHRs were given orally and for 8 days either losartan (10 mg kg-' daily) or distilled water (controls).After pithing, blood pressure, heart rate, cardiac output, renal and muscular blood flows (pulsed Doppler technique) and the corresponding vascular resistance values were measured or calculated at baseline. Then, animals from both groups were given i.v. either saline, or NG-nitro-L-arginine methyl ester (L-NAME, 1 mg kg-1), or diclofenac (4 mg kg-'). Thereafter, haemodynamic parameters were determined in the six subgroups of animals in response (a) to SCS at increasing frequencies, and (b) to a noradrenaline bolus injection. 3 Losartan significantly decreased mean arterial pressure as well as renal and total peripheral resistances. In addition, losartan exhibited strong vascular sympathoinhibitory effects, significantly decreasing the systemic pressor and regional vasoconstrictor responses to SCS, but did not affect those to exogenous noradrenaline. In contrast, SCS-induced tachycardia was not modified by losartan. 4 L-NAME significantly increased total peripheral and regional vascular resistances but did not affect blood pressure and heart rate basal values. L-NAME potentiated the haemodynamic responses to SCS in control and, to a larger extent, in losartan-treated SHRs so that, with the exception of the renal vascular bed, the sympathoinhibitory effects of losartan were attenuated in all vascular beds studied. L-Arginine (300 mg kg-1) caused reversal of L-NAME effects in both control and losartan-treated SHRs. 5 Diclofenac did not affect the basal values of haemodynamic parameters in control and losartantreated SHRs. Diclofenac potentiated the pressor and vasoconstrictor responses to SCS and to a similar extent, in both control and losartan-treated SHRs, so that the sympathoinhibitory effects of losartan were fully maintained. 6 These results demonstrate that in pithed SHRs: (a) NO but not PGs contribute to the basal vasomotor tone, (b) both NO and PGs attenuate the pressor and vasoconstrictor responses to SCS, (c) NO plays a major role in the vascular sympathoinhibitory effects of losartan, except at the renal level, and (d) endogenous PGs are not involved in these sympathoinhibitory effects.

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Section: Discussionsupporting

confidence: 60%

Involvement of nitric oxide, but not prostaglandins, in the vascular sympathoinhibitory effects of losartan in the pithed spontaneously hypertensive rat

Richer

Domergue

Vincent

et al. 1996

British J Pharmacology

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“…However, when hemorrhage was assessed by quantifying the amount of hemoglobin in muscle tissue, no differences were observed between the various experimental groups. This discrepancy may be related to the marked heterogeneity of the action of NO in the microvasculature of various organs [40]. It is suggested that the effect in skin may be secondary to the alterations resultant from NO synthase inhibition in hemodynamic parameters.…”

Section: Discussionmentioning

confidence: 99%

Role of nitric oxide in the local and systemic pathophysiological effects induced by Bothrops asper snake venom in mice

2006

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Abstract.Objective: To assess the role of nitric oxide in the most relevant local and systemic manifestations in mice injected with the venom of the snake Bothrops asper. Mice were pretreated with nitric oxide synthase inhibitors, and the modifi cations of the pathological effects induced by the venom were tested. Results: Inhibition of NO synthesis did not affect acute local myonecrosis and hemorrhage in muscle tissue upon intramuscular injection of venom. Local footpad edema was reduced in mice pretreated with the NO synthase inhibitor L-NAME, and a reduction in the extent of infl ammatory infi ltrate in muscle tissue was observed after envenomation in mice pretreated with L-NAME and aminoguanidine. The most pronounced effect of NOS inhibition by L-NAME was an increment in the lethal activity of the venom, when injected by the intraperitoneal route. Conclusion: Nitric oxide does not seem to play a signifi cant role in the local acute pathological alterations (hemorrhage and myonecrosis) induced by B. asper venom in mice, although it contributes to edema and infl ammatory infi ltrate. Nitric oxide exerts a protective role in the systemic pathophysiological manifestations leading to lethality.

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“…NO seems to function as a local vasodilator in the gastric mucosal microvasculature, although the relative contributions of neurogenic and endothelial NO have not been determined. NOS inhibitors also decreased the vascular conductance in the mesenteric vascular bed (Greenblatt et al, 1993;Macedo and Lautt, 1997).…”

Section: Digestive Tract Vasculaturementioning

confidence: 90%

“…CGRP was reportedly the sole transmitter for vasodilation in rat hepatic artery (Bratveit and Helle, 1991). In anesthetized cats, L-NAME raised basal vascular tone in the superior mesenteric artery but not in the hepatic artery, suggesting 292 that the role of endogenous NO is, if any minimal, in hepatic vasculature (Greenblatt et al, 1993;Macedo and Lautt, 1997).…”

Section: Digestive Tract Vasculaturementioning

confidence: 98%

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

2003

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Marked Regional Heterogeneity in the Magnitude of EDRF/NO-Mediated Vascular Tone in Awake Rats

Cited by 55 publications

References 0 publications

Involvement of nitric oxide, but not prostaglandins, in the vascular sympathoinhibitory effects of losartan in the pithed spontaneously hypertensive rat

Involvement of nitric oxide, but not prostaglandins, in the vascular sympathoinhibitory effects of losartan in the pithed spontaneously hypertensive rat

Role of nitric oxide in the local and systemic pathophysiological effects induced by Bothrops asper snake venom in mice

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

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