What is the relationship between the endothelium derived relaxant factor and nitric oxide?

Long, Clive; Berkowitz, Barry A.

doi:10.1016/0024-3205(89)90429-3

Cited by 27 publications

(8 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The finding that hindquarters vasodilator responses to acetylcholine (this paper) and to endothelin-1 (Kiff et al, 1991) were intact when bradykinin-mediated responses were impaired in STZ-treated rats is consistent with the relative resistance of the former responses to inhibition by L-NAME (Gardiner et al, 1990b). Elsewhere (Gardiner et al, 1990b) we have discussed the possibility that this is due to release of nitric oxide from a pre-formed pool and/or the involvement of nitric oxide-independent mechanisms (Aisaka et al, 1989;Long & Berkowitz, 1989).…”

Section: Discussionsupporting

confidence: 52%

Selective impairment of hindquarters vasodilator responses to bradykinin in conscious Wistar rats with streptozotocin‐induced diabetes mellitus

Kiff

Gardiner

Compton

et al. 1991

British J Pharmacology

View full text Add to dashboard Cite

1 Male, Wistar rats were treated with streptozotocin (STZ, i.p.) or saline and chronically instrumented with pulsed Doppler probes and intravascular catheters (implanted under sodium methohexitone anaesthesia) to allow assessment of haemodynamics in the conscious state 28 days later. 2 Control and STZ-treated rats received bolus doses of glyceryl trinitrate (10-80 nmol kg 1), acetylcholine (0.1-5 nmol kg-1) and bradykinin (0.3-30 nmol kg-1).3 Although, as reported previously, STZ-treated rats had normal mean arterial blood pressure together with renal and mesenteric vasodilatations and hindquarters vasoconstriction relative to control rats, both groups showed similar hypotensive and regional haemodynamic responses to glyceryl trinitrate and acetylcholine. However, while the depressor effects of bradykinin were similar in control and STZ-treated rats, the former showed a hindquarters vasodilator response to bradykinin that was absent in the STZtreated rats. 4 A loss of bradykinin-mediated vasodilatation in the hindquarters vascular bed in STZ-treated rats in the presence of normal, hindquarters vasodilator responses to other agents and normal bradykininmediated vasodilator responses in other vascular beds is consistent with existing evidence that the vasodilatation elicited by bradykinin in the hindquarters vascular bed is particularly dependent on nitric oxide synthesis and that this is impaired selectively in STZ-treated rats.

show abstract

Section: Discussionsupporting

confidence: 52%

Selective impairment of hindquarters vasodilator responses to bradykinin in conscious Wistar rats with streptozotocin‐induced diabetes mellitus

Kiff

Gardiner

Compton

et al. 1991

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…While these results indicate a component of the control response to acetylcholine was probably due to nitric oxidemediated mechanisms, substantial responses remained under these conditions, and, in particular, the hindquarters vasodilator response was not different from normal. There are several possible explanations for these findings, including: (1) the responses were due to a mechanism not involving nitric oxide (see Long & Berkowitz, 1989); (2) the responses were due to release of nitric oxide from a preformed pool (see Aisaka et al, 1989); (3) the responses were due to nitric oxide, but relatively unaffected by L-NAME due to efficient receptor-effector coupling (Giles et al, 1990). Considering this last possibility we have carried out preliminary experiments to assess the effect of atropine on the sensitivity of acetylcholine-induced vasodilator responses to L-NAME (Giles et al, 1990).…”

Section: Responses To Acetylcholinementioning

confidence: 99%

Regional and cardiac haemodynamic responses to glyceryl trinitrate, acetylcholine, bradykinin and endothelin‐1 in conscious rats: effects of N^G‐nitro‐l‐arginine methyl ester

Gardiner

Compton

Kemp

et al. 1990

British J Pharmacology

133

111

View full text Add to dashboard Cite

1 Conscious Long Evans rats, chronically instrumented for cardiovascular measurements, were challenged with i.v. bolus doses of glyceryl trinitrate (40 nmol kg-1), acetylcholine (1.2 nmol kg-1), bradykinin (3.2 nmol kg-1), or endothelin-1 (0.25 nmol kg '). Under control conditions these doses produced similar falls in mean arterial blood pressure (glyceryl trinitrate, -20 + 3 mmHg; acetylcholine, -24 + 2 mmHg; bradykinin, -21 + 3 mmHg; endothelin-1, -25 + 3 mmHg), associated with renal, mesenteric and hindquarters vasodilatations (except for endothelin-1 which caused mesenteric vasoconstriction). 2 In the presence of NG-nitro-L-arginine methyl ester (L-NAME, 10 mg kg-1), a potent inhibitor of nitric oxide biosynthesis and endothelium-dependent vasorelaxation in vitro, the hypotensive responses to glyceryl trinitrate, acetylcholine, and endothelin-1 were increased, although that to bradykinin was not. However, comparing the differences between the response to glyceryl trinitrate and that to any other agonist in the absence and presence of L-NAME showed that there were relative attenuations of the hypotensive responses to bradykinin and endothelin-1, but not to acetylcholine, in the presence of L-NAME. 3 This comparative analysis showed that the renal and hindquarters vasodilator responses to bradykinin and endothelin-1 were attenuated in the presence of L-NAME, but the renal, mesenteric and hindquarters vasodilator responses to acetylcholine were not. However, when L-NAME was administered in the presence of pentolinium, captopril and the vasopressin Vj-receptor antagonist, d(CH2)5[Tyr-(Et)]DAVP, (to abolish baroreflex and neurohumoral mechanisms), there was attenuation of the renal and mesenteric vasodilator effects of acetylcholine relative to those seen with glyceryl trinitrate. Under those conditions only the renal vasodilator effects of bradykinin and endothelin-1 were attenuated. 4 In separate experiments in conscious Long Evans rats, direct measurement of cardiac haemodynamics showed that the hypotensive responses to glyceryl trinitrate, acetylcholine, bradykinin and endothelin-l were entirely attributable to rises in total peripheral conductance since both in the absence and presence of L-NAME there were no reductions in cardiac index in response to these substances. 5 The results indicate that measurement of systemic arterial blood pressure alone in conscious rats does not permit reliable quantitation of the influence of L-NAME on regional vasodilator responses to glyceryl trinitrate, acetylcholine, bradykinin or endothelin-1. Furthermore, these substances exert effects in different vascular beds that may be differentially influenced by baroreflex mechanisms, neurohumoral mechanisms, or both. Moreover, except in the case of the renal vasodilator response to endothelin-1 (which was abolished in the presence of L-NAME), even when L-NAME caused attenuation of the vasodilator effects of acetylcholine or bradykinin (relative to glyceryl trinitrate), substantial responses remained. It is feasible that such r...

show abstract

“…The endothelial cells, however, were NADPH-dpositive and could suggest the presence of NO. The vasodilator role of NO in endothelial cells is well known through its inhibitory action on vascular smooth muscle (Ignarro et al 1987;Amezcua et al 1988;Long and Berkowitz 1989). NO-mediated vasodilation not only could occur in endothelial cells, but also through nitrergic nerves acting directly on smooth muscle cells (Burnett et al 1992;Kummer et al 1992).…”

Section: Discussionmentioning

confidence: 99%

Histochemical and immunohistochemical localisation of nitrergic neuronal and non-neuronal cells in the bursa of Fabricius of the chicken

Ali

Chan

Leong

1996

Cell and Tissue Research

View full text Add to dashboard Cite

The bursa of Fabricius of 24 chickens, 2-4 weeks old, was investigated to determine the distribution of nicotinamide adenine dinucleotide hydrogen phosphate-diaphorase (NADPH-d) staining and nitric oxide synthase (NOS) antigen, by use of NADPH-d histochemistry and NOS immunohistochemistry, respectively. NADPH-d reaction product was localised in neuronal cell bodies and nerve fibres. The stained cell bodies were predominantly in the different bursal compartments; some occurred in the wall and between the lymphoid follicles, and some in the immediate vicinity of blood vessels. Stained nerve fibres travelled mostly with blood vessels, but many were also observed in the connective tissue of the bursa, independent of blood vessels, and some in contact with the lymphoid follicle and interfollicular epithelium. In addition to neuronal profiles, the interfollicular epithelium of the plicae, and the vascular endothelium were densely stained, and lymphocytes were moderately labelled. NOS immunoreactivity was found in neuron-like cells and fibres which were confirmed to be neuronal in adjacent sections stained with antibodies raised against neuron-specific enolase. It was also detected in interfollicular epithelium and lymphocytes but not in vascular endothelium. The distribution patterns of NADPH-d and NOS suggest that nitric oxide (NO) may play a role in the regulation of the secretory activity of interfollicular epithelium and the blood flow through the bursa.

show abstract

What is the relationship between the endothelium derived relaxant factor and nitric oxide?

Cited by 27 publications

References 29 publications

Selective impairment of hindquarters vasodilator responses to bradykinin in conscious Wistar rats with streptozotocin‐induced diabetes mellitus

Selective impairment of hindquarters vasodilator responses to bradykinin in conscious Wistar rats with streptozotocin‐induced diabetes mellitus

Regional and cardiac haemodynamic responses to glyceryl trinitrate, acetylcholine, bradykinin and endothelin‐1 in conscious rats: effects of N^G‐nitro‐l‐arginine methyl ester

Histochemical and immunohistochemical localisation of nitrergic neuronal and non-neuronal cells in the bursa of Fabricius of the chicken

Contact Info

Product

Resources

About

What is the relationship between the endothelium derived relaxant factor and nitric oxide?

Cited by 27 publications

References 29 publications

Selective impairment of hindquarters vasodilator responses to bradykinin in conscious Wistar rats with streptozotocin‐induced diabetes mellitus

Selective impairment of hindquarters vasodilator responses to bradykinin in conscious Wistar rats with streptozotocin‐induced diabetes mellitus

Regional and cardiac haemodynamic responses to glyceryl trinitrate, acetylcholine, bradykinin and endothelin‐1 in conscious rats: effects of NG‐nitro‐l‐arginine methyl ester

Histochemical and immunohistochemical localisation of nitrergic neuronal and non-neuronal cells in the bursa of Fabricius of the chicken

Contact Info

Product

Resources

About

Regional and cardiac haemodynamic responses to glyceryl trinitrate, acetylcholine, bradykinin and endothelin‐1 in conscious rats: effects of N^G‐nitro‐l‐arginine methyl ester