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At least 19 recordsLinked to original sources
PubMed1989

S-nitrosothiols as vasodilators: implications regarding tolerance to nitric oxide-containing vasodilators.

1. The formation of an S-nitrosothiol compound, S-nitroso-N-acetylcysteine (SNAC) has recently been proposed to mediate the augmentation of the anti-aggregatory and haemodynamic effects of glyceryl trinitrate observed in the presence of N-acetylcysteine. This study investigated the effects on an isolated coronary artery preparation of acute and prolonged exposure to S-nitrosothiol compounds and nitric oxide (NO). 2. Single doses of NO and of the S-nitrosothiol compounds, SNAC and S-nitroso-N-acetyl-penicillamine (SNAP), induced rapid, but transient, relaxations in U46619-contracted bovine isolated coronary artery rings. Peak relaxation responses to SNAP and NO were attenuated in the presence of N-acetylcysteine, cysteine, ascorbic acid and methylene blue. The duration of the relaxation responses to SNAC was two to three times longer than those to SNAP and NO. In the presence of N-acetylcysteine (but not cysteine, ascorbic acid or methylene blue) the duration of the relaxation responses to SNAP and NO (but not to SNAC) was markedly increased. H.p.l.c. assay confirmed that, in the presence of N-acetylcysteine, SNAP and, to a lesser degree, NO were converted to the relatively more stable and longer acting vasodilator, SNAC. 3. When compared to control rings, coronary artery rings superfused with glyceryl trinitrate were subsequently markedly less responsive to the vasodilator actions of glyceryl trinitrate, whereas responsiveness to SNAC or NO was only marginally reduced. On the other hand, coronary artery rings superfused with SNAC or NO were subsequently less responsive to glyceryl trinitrate, SNAC and NO. Thus prolonged vascular exposure to SNAC or NO induced a form of tolerance different from that induced with glyceryl trinitrate and which is possibly associated with impaired guanylate cyclase activity. 4. Coronary artery rings superfused with NO were markedly less responsive to glyceryl trinitrate and NO, whereas responses to the endothelium-dependent vasodilator A23187 and to theophylline were not significantly attenuated. 5. It is concluded that formation of the more stable vasodilator SNAC occurs on incubation of N-acetylcysteine with SNAP or NO. While coronary artery responsiveness to SNAC and NO is virtually unchanged in the presence of glyceryl trinitrate-induced tolerance, after prolonged exposure to SNAC or NO tolerance may develop to these vasodilators with cross-tolerance to glyceryl trinitrate but not A23187. Thus, formation or therapeutic utilization of SNAC may acutely circumvent the problem of glyceryl trinitrate-induced tolerance but, during prolonged vascular exposure to SNAC, attenuation of vascular responsiveness may occur to a wide range of vasodilators.

Acetylcysteine↗
PubMedDate not supplied

The influence of dihydroergotamine on adenosine-induced and reactive coronary vasodilation. Interaction of dihydroergotamine and coronary vasodilation.

The influence of dihydroergotamine on adenosine-induced and reactive vasodilation after long and short periods of coronary artery occlusion was investigated in thoracotomized dogs. Adenosine-induced vasodilation (intracoronary administration) and vasodilation after long periods of coronary artery occlusion (25-35 beats) were similarly influenced, i.e. decreased by the i.v. administration of 10 mug/kg dihydroergotamine. By contrast vasodilation after short periods of coronary artery occlusion (4-7 beats) tended to be increased. This difference in response is thought to arise from two distinct mechanisms of coronary vasodilation after coronary artery occlusion depending on the duration of the occlusion period. The vasodilation after short periods of coronary artery occlusion possibly corresponds to physiological autoregulation. With longer periods of coronary artery occlusion an additional, consecutive mechanism is called into action.

Adenosine↗
PubMed1985

The effectiveness of local injections of vasodilating agents to produce vasodilation in subcutaneous tissue in rabbits.

The isotope washout method has been widely used to study characteristics of the microcirculation in localized vascular beds. Some of these studies have used local injections of vasodilating agents to maximally dilate the vascular bed. This study was undertaken to determine the agent most effective in producing this critical vasodilation. A rabbit model was constructed that allowed the study of the subcutaneous blood flow by either 133Xe and 131I-antipyrine washout. Dose-response curves were constructed for five agents. The agents used and the doses that produced the maximum washout rate, were histamine (100 micrograms), verapamil (0.5 mg), prostaglandin E1 (6 micrograms), papaverine (5 mg) and nitroprusside (60 micrograms). The five agents at these doses were compared with each other, and nitroprusside produced a greater washout rate than papaverine (P less than 0.005), histamine (P less than 0.001) and verapamil (P less than 0.005). There was no difference between nitroprusside and prostaglandin E1 (P greater than 0.01). The effect of three of the agents in producing tissue oedema was examined by comparing the washout rates values obtained with the two isotopes. Both nitroprusside and papaverine produced large oedema whereas histamine resulted in little oedema formation. Nitroprusside, therefore, appears to be the most suitable vasodilating agent for use in studies which require maximum vasodilation of localized vascular beds.

Alprostadil↗
PubMed1988

Pinacidil-induced vascular relaxation: comparison to other vasodilators and to classical mechanisms of vasodilation.

Pinacidil is a potent antihypertensive agent in animals and humans. In conscious spontaneously hypertensive rats after oral administration, pinacidil was approximately 3- and 10-fold more potent than hydralazine and minoxidil, respectively. Likewise, under in vitro conditions, pinacidil (ED50 = 0.3 microM) was more potent in relaxing serotonin-contracted rat aortic strips than either minoxidil (ED50 = 0.1 mM) or hydralazine (ED50 = 0.2 mM). These data are consistent with the contention that pinacidil is a direct-acting vasodilator whereas minoxidil and hydralazine may be converted in vivo to active moieties and/or exert indirect effects more apparent under in vivo than in vitro conditions. The pharmacology of pinacidil appears unrelated to classical mechanism of vasodilation. Pinacidil does not interact with alpha, beta, cholinergic, or histaminergic receptors. Pinacidil does not produce vasodilation via an indirect effect mediated by adenosine, prostaglandin, or endothelial-derived relaxant factor (EDRF) release. Pinacidil does not alter cAMP or cGMP levels and, based on numerous approaches, does not resemble conventional calcium channel antagonists in its vasodilating activity. Thus, a review of the literature presented herein supports the contention that pinacidil-induced vascular relaxation is a direct effect mediated by a novel mechanism.

Animals↗
PubMed1992

Effects of chronic administration of antihypertensive drugs on vasodilation mediated by calcitonin gene-related peptide-containing vasodilator nerves in spontaneously hypertensive rats.

1. The effects of chronic administration of antihypertensive drugs on the vasodilator response mediated by calcitonin gene-related peptide (CGRP)-containing nerves were investigated in spontaneously hypertensive rats (SHR). 2. A 7 week period of antihypertensive treatment with captopril, nicardipine or propranolol during the developmental phase (8-15 weeks of age) significantly lowered the mean blood pressure of SHR when compared with non-treated SHR. 3. The mesenteric vascular beds isolated from SHR, which were chronically administered with captopril, propranolol or nicardipine, were perfused with Krebs' solution containing 7 mumol/L methoxamine to produce active tone and 5 mumol/L guanethidine to block adrenergic neurotransmission. 4. In the mesenteric vascular bed with active tone, perivascular nerve stimulation (PNS; 0.5-8 Hz) caused a frequency-dependent vasodilator response that was abolished by 100 nmol/L tetrodotoxin (neurotoxin) or 1 mumol/L CGRP (8-37), a CGRP receptor antagonist. 5. CGRP-containing nerve-mediated vasodilator responses were significantly greater in captopril-treated SHR and significantly smaller in nicardipine-treated SHR than in non-treated SHR. There was no difference between the response between propranolol-treated SHR and non-treated SHR. 6. These results suggest that chronic treatment with captopril reverses the reduced neurogenic vasodilation mediated by CGRP-containing nerves in SHR.

Animals↗
PubMed1979

Effects of coronary vasodilator on cyclic nucleotides. The concentrations of cyclic AMP and cyclic GMP in canine coronary artery and left ventricular muscle following the administration of various coronary vasodilators.

We examined the effects of various coronary vasodilator drugs, papaverine, dipyridamole, isosorbide dinitrate, amyl nitrite, nitroglycerin, diltiazem, and nifedipine, on cyclic nucleotides of the coronary artery and left ventricular muscle of anesthetized dogs at maximum coronary blood flow after the administration of each agents. Only papaverine and dipyridamole significantly increased the concentration of c-AMP in the coronary artery. Nitroglycerin and siosorbide dinitrate did not significantly change the concentration of c-AMP but rather increased the concentration of c-GMP. Coronary vasodilator drugs were divided into three groups in association with the relationship of cyclic nucleotides in the coronary artery. Group I, including papaverine, dipyridamole, and amyl nitrite, increased the concentration of c-AMP and the ratio of c-AMP to c-GMP. Group II, including nitroglycerin and isosorbide dinitrate, incrased the concentration of c-GMP and decreased the ratio of c-AMP to c-GMP. Group III, including nifedipine and diltiazem, had no effect on the cyclic nucleotides. Group I drugs also increased the concentration of c-AMP in the left ventricular muscle and so group I drugs may predispose the ischemic heart to develop ventricular arrhythmias. It seems that the most useful coronary vasodilator is no effect on the c-AMP in the ventricular muscle and group II and group III drugs are more useful coronary vasodilator drugs than group I drugs.

Amyl Nitrite↗
PubMed1989

Renal vasodilators. The role of the 4-substituent in isoquinolin-3-ol cardiovascular agents: 4-ureido derivatives of isoquinolin-3-ol with selective renal vasodilator properties.

The synthesis and cardiovascular evaluation of a series of isoquinolin-3-ol derivatives bearing a variety of nitrogen substituents (amino, acylamino, carbamate, and ureido) at C-4 are described. Certain of these compounds have a selective renal vasodilating profile and have minimal effects on arterial blood pressure or heart rate when administered intravenously in the instrumented anesthetized dog. The most potent renal vasodilator in the series is 4-(allylureido)-6,7-dimethoxyisoquinolin-3-ol (38), which at a dose of 1.2 mg/kg iv produces a 97% maximal increase in renal blood flow without significant hypotensive or chronotropic effects. Structure-activity observations on the nature of the 4-substituent and the alkoxy substitution pattern in the aromatic ring of the isoquinolinol nucleus are discussed.

Animals↗
PubMed1985

Vasodilators in hypertension--a review with special emphasis on the combined use of vasodilators and beta-adrenoceptor blockers.

This paper presents a review of studies dealing with combined beta-adrenoceptor blockade and vasodilatation in the treatment of hypertension. This therapy can be achieved either through the combined use of conventional beta-adrenoceptor blocking compounds given together with vasodilator drugs or with agents which show multiple action of this kind. From a hemodynamic point of view this therapeutic approach is quite logical since most forms of established hypertension are characterized by increased vascular resistance. It can therefore be concluded that combined beta-adrenoceptor blockade and vasodilation offers a rational and useful treatment of hypertension.

Adrenergic alpha-Antagonists↗
PubMed1978

[The treatment of congestive heart failure by using vasodilators. I. Physiological basis. Different vasodilators (author's transl)].

The use of vasodilators represents a new approach in the treatment of heart failure. These drugs have the property of causing vasodilatation of either arterial or venous predominance or balanced between these two vascular beds. Arterio-dilators (phentolamine, hydralazine) increase stroke volume and cardiac output by decreasing ventricular afterload. Veno-dilators (nitroglycerine) have little effect on cardiac output but decrease ventricular filling pressure, thereby relieving pulmonary venous hypertension. Mixed vasodilators (Sodium nitroprussideate, trimetaphan) combine these two groups of properties in various degrees. The majority of these drugs can only be administered intravenously, with careful haemodynamic surveillance.

Cardiac Output↗
PubMed1992

Endothelium-dependent vasodilation by LP-805, a novel vasodilating agent, on rat thoracic aorta.

1. In rat aortae with [E(+)-tissue] and without [E(-)-tissue] intact endothelium, LP-805 relaxed the preparations precontracted with 35.9 mM K+ and its action in E(+)-tissues was more potent than that in E(-)-tissues. Moreover, the inhibitory action of glibenclamide in E(-)-tissues was more potent than that in E(+)-tissues. 2. The relaxing action of LP-805 on E(+)-tissues treated with NG-nitro-L-arginine methyl ester (10 microM), a potent inhibitor of nitric oxide synthesis, was the same as that in E(-)-tissues. 3. Methylene blue (10 microM) also inhibited the LP-805 induced relaxation in E(+)-tissues. 4. Indomethacin (10 microM) had no effect on LP-805-induced relaxation in E(+)-tissues. 5. These results suggest that the vasorelaxant action of LP-805 involves the mechanism which causes the release of nitric oxide (NO) from vascular endothelium.

Animals↗
PubMed1976

[Comparative study of acoustic trauma caused by blasts, treated by vasodilators or by a combination of vasodilators and hyperbaric oxygenation].

The authors had comparated two series of patients with noise induced hearing loss treated by vasodilatators or vasodilatators and hyperbaric oxygen. This therapy seems to give better results than the vasodilatators only, but the patients had to be treated before ten days after the noise exposition. In the two series of acoustic trauma we see rarely a complete recovery from the hearing loss.

Adult↗