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At least 19 recordsLinked to original sources
PubMed1988

[Therapy of heart failure with vasodilator agents].

Vasodilation in congestive heart failure is an established therapeutic principal. The ventricular unloading improves contractile geometry and thereby improves working conditions for the contractile element: myocardial oxygen consumption falls and myocardial efficiency improves. This effect is independent from the vasodilating substance employed; it is, however, dependent on the simultaneous induction of pre- and afterload reduction. Vasodilation improves regional perfusion. Differential improvement in organ bloodflow is related to the type of vasodilator employed. It seems essential for a therapeutic benefit that renal and coronary perfusion are improved and that shunt flow, especially with steal phenomena, is avoided. Skeletal muscle bloodflow improves only slowly under ACE-inhibitor therapy. It could be shown that the immediate vasodilation due to ACE inhibition is followed by a second phase of vasodilation, which may be related to the influence of ACE inhibition of intraarterial wall angiotensin converting enzyme. Another factor possibly responsible for the delayed response to vasodilation in congestive heart failure, may be functional and structural changes in skeletal muscle. Reversal of these changes requires time. Both factors - the vessel wall related mechanism, as well as changes in parenchymal structure and function - require prolonged periods of treatment until therapeutic benefit can be seen.

Angiotensin-Converting Enzyme Inhibitors↗
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↗
PubMed1996

The effect of topical vasodilating agents on microvascular vessel diameter in the rat model.

Topical vasodilating agents maximize blood flow and prevent vasospasm in microvascular tissue-transfer procedures. Two commonly used agents are papaverine and lidocaine. Although these drugs have vasodilating properties, no studies have directly compared their vasodilating abilities in a controlled, in vivo model. We used videomicroscopy and direct microscopic measurements to compare the vasodilating capacity of papaverine, 1% lidocaine, and saline solution in the femoral artery of Sprague-Dawley rats. Degree of maximum dilation, ability to sustain dilation, average dilation over a 10-minute period, and time to achieve maximum dilation were considered. Both papaverine and lidocaine were found to be superior to saline solution as vasodilating agents. Papaverine was found to sustain vasodilation longer than lidocaine, suggesting that it is a superior vasodilating agent in microvascular anastomoses.

Administration, Topical↗
PubMed1994

In vitro femoral arterial responses to vasoconstrictor and vasodilator agents in endotoxin shock.

The hypothesis for this study is that the decreased arterial response to catecholamines may be due to the effect of endotoxemia on vessel tone. One control ring was taken from one femoral artery of a Wistar rat and after endotoxin (ENDT) infusion (i.v. 6 mg/kg-1 hr.), one ring was removed from the contralateral artery. The post-ENDT rings were tested in four groups which were determined by the mean arterial pressure (MAP) levels at the time of dissection: 100 mmHg (120 min), 80 mmHg (270 min), 60 mmHg (300 min) or 40 mmHg (330 min). KCl, phenylephrine (PHE) and arginine-vasopressin (AVP) dose-response curves (DR) were obtained at a preload of 500 mg which allowed the maximum response in control rings. When compared at 500 mg preload the maximal active response to all agonists post-ENDT was decreased by about 50%. By increasing the preload on the ENDT rings to 800 mg, the active tension became 2.49 times the active tension of the control rings. Length-tension experiments also showed a greater response for post-ENDT rings and a greater preload at maximum response but the ring circumference was the same. In contrast the in vivo femoral artery diameters at 90 min post-ENDT (100 mmHg) were 82.6% of control. Endothelium-dependent relaxation by acetylcholine (ACh) was abolished by ENDT but endothelium-independent relaxation to nitroprusside (NP) was not affected. It is concluded that the resting tone and active tension of femoral artery smooth muscle is increased by ENDT and the decreased in vivo responsiveness to vasoconstrictor agonists may be the result of vessel constriction due to loss of endothelium. The results also suggest that in vitro comparison of vessels in studies of endotoxin shock be done at the same muscle length rather than at the same preload.

Acetylcholine↗
PubMed1986

Hypertension alters slope and range but not sensitivity to vasoconstrictor and vasodilator agents in the rabbit hindquarter.

The vascular reactivity (slope and range) and location parameter (ED50) of dose-response curves in the hindquarter vascular bed in conscious rabbits previously subjected to renal cellophane wrapping or sham operation were examined. The animals were instrumented with pulsed Doppler flow transducers and chronic indwelling aortic catheters for intra-arterial drug infusion. The rabbits were ganglion-blocked with mecamylamine before constructing full dose-response curves to intra-arterial infusions of methoxamine, noradrenaline, angiotensin II, acetylcholine, adenosine and serotonin. Curves relating dose to conductance were fitted to the experiments involving constrictors and curves relating dose to vascular resistance fitted to those involving dilator drugs. With both classes of drugs the reactivity was significantly higher in the hypertensive animals than in sham-operated rabbits. There was no difference in sensitivity (ED50 value) between the hypertensive and control animals for any agonist tested. The increased reactivity, but not sensitivity, could be entirely accounted for by the vascular amplifier action of medial hypertrophy in hypertension.

Animals↗
PubMedDate not supplied

Responses of rabbit basilar arteries to vasoconstrictor and vasodilator agents: the effects of atherosclerosis, age and sex.

We have studied the influences of atherosclerosis, age and sex on arterial responsiveness to vasoactive agents using male and female Watanabe heritable hyperlipidaemic (WHHL) rabbits (4-12 months, n = 36) as a model for atherosclerosis and sex- and age-matched New Zealand White (NZW) rabbits (n = 36) as controls. The responses of isolated rings of basilar arteries mounted in organ baths to vasoactive substances were studied. KCl-induced contractions in female atherosclerotic rabbits were greater than controls but those of male atherosclerotic rabbits were equivalent to the respective controls. Age did not influence KCl-induced contractions of rabbits of either strain or sex. Histamine-induced contractions increased with age in female atherosclerotic rabbits only. Acetylcholine (ACh)-induced relaxations of 6-month-old male and female atherosclerotic rabbits were greater than their respective controls. ACh-induced relaxations of female but not male NZW rabbits decreased with age. Calcitonin gene-related peptide- and vasoactive intestinal polypeptide-induced relaxations in atherosclerotic male and female rabbits were not affected by age. However, relaxations of female but not male control rabbits decreased with age. These findings suggest that there are subtle changes in the control of vascular tone which develop with the onset and progression of atherosclerosis. Of particular significance is the increase in endothelium-dependent relaxation in WHHL rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Vasodilator agents modulate rat glomerular mesangial cell growth and collagen synthesis.

Mesangial cell activation and extracellular matrix accumulation are hallmarks of many forms of glomerulonephropathy. We investigated the effect of several agents possessing vasodilating activities on rat mesangial cell growth and collagen synthesis. Using cell counting and a modified MTT assay, it was shown that dipyridamole, pentoxifylline, dicentrine, prazosin and doxazosin all caused a dose-dependent inhibition of serum-stimulated rat mesangial cell proliferation. Platelet-derived growth factor-induced cell proliferation was also inhibited by doxazosin and pentoxifylline. Dipyridamole and pentoxifylline inhibited collagen synthesis in confluent mesangial cells while dicentrine and doxazosin did not. The procollagen alpha 1 (I) mRNA expression was also decreased by dipyridamole and pentoxifylline. These results suggested that, in addition to dipyridamole, pentoxifylline and alpha 1-adrenoceptor blockers may have a potential to delay the progression of chronic glomerulopathy associated with mesangial proliferation.

Analysis of Variance↗
PubMed1977

Influence of inhibitors of prostaglandin synthesis on renal vascular resistance and on renal vascular responses to vasopressor and vasodilator agents in the cat.

We determined the effects of indomethacin and meclofenamate, two inhibitors of prostaglandin synthesis, on renal vascular resistance and on renal responses to nerve stimulation, pressor and depressor hormones in the in situ feline kidney under conditions of controlled blood flow. Both inhibitors produced a gradual rise in renal vascular resistance which became maximal 15-20 minutes after administration. The increase in renal resistance after indomethacin was not attenuated during intrarenal infusion of either phentolamine or SQ 20881. Pretreatment with propranolol, in a dose sufficient to inhibit renin secretion, also did not attenuate the increase in renal resistance produced by indomethacin. However, infusion of [Sar1-, Ala8]angiotensin II, an angiotensin II antagonist, did attenuate the indomethacin-induced increase in renal vascular resistance. After indomethacin, the vasoconstrictor response to norepinephrine was enhanced, whereas responses to nerve stimulation and angiotensin were unaffected. Although meclofenamate enhanced renal vascular resistance, its effects on vasoconstrictor responses were inconsistent. After indomethacin, the renal dilator response to bradykinin was enhanced; however, dilator responses to nitroglycerin were unaltered. The present data indicate that the increase in renal vascular resistance after indomethacin does not depend on the adrenergic system but may be dependent on the renin-angiotensin system. The inconsistent effect of the inhibitors of synthesis on renal constrictor responses to nerve stimulation suggests that endogenous prostaglandins do not serve to modulate the effects of the sympathetic nervous system on the feline renal vascular bed. These results also indicate that renal dilator responses to bradykninin are not mediated by prostaglandins in the cat.

Animals↗
PubMed1990

Effects of vasoconstrictive and vasodilative agents on lymphatic smooth muscles in isolated canine thoracic ducts.

A study was made of the isometric responses of isolated canine thoracic ducts to several physiological vasoactive substances. Contractions of the lymphatic smooth muscles were induced by epinephrine, norepinephrine, 5-hydroxytryptamine, histamine (HIS) and prostaglandin F2 alpha in a dose-dependent manner. The decreasing order of potency in the contractile responses was as follows: epinephrine greater than norepinephrine greater than 5-hydroxytryptamine much greater than HIS not equal to prostaglandin F2 alpha. There were no significant regional differences in the responses to vasoconstrictive agents. Phenylephrine, xylazine and clonidine caused a dose-dependent contraction in the lymphatic preparations. Prazosin (10(-8) to 10(-7) M) inhibited the phenylephrine-induced vasoconstriction in a competitive manner. Xylazine-induced responses were inhibited competitively by yohimbine (10(-8) to 10(-7) M). These results suggest that both alpha-1 and alpha-2 adrenoceptors are located on the lymphatic smooth muscles of canine thoracic ducts. On the other hand, acetylcholine, isoproterenol, HIS, adenosine and ATP caused dose-dependent relaxations in canine thoracic ducts precontracted by 10(-5) M norepinephrine. The decreasing order of potency in the relaxant responses was as follows: acetylcholine much greater than isoproterenol much greater than adenosine not equal to HIS not equal to ATP. There were no significant regional differences in the relaxant responses to the agents. Procaterol, salbutamol, dobutamine and denopamine caused a dose-dependent relaxation of isolated canine thoracic ducts. Propranolol (10(-9) to 10(-8) M) inhibited procaterol- and dobutamine-induced vasorelaxations in a competitive manner. Metoprolol (10(-8) to 10(-7) M) inhibited only the dobutamine-induced vasorelaxation, but did not significantly influence the procaterol-induced response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Beta-adrenergic blocking agents in heart failure: benefits of vasodilating and non-vasodilating agents according to patients' characteristics: a meta-analysis of clinical trials.

BACKGROUND: In patients with heart failure, beta-adrenergic blocking agents reduce overall and cardiovascular mortality. This meta-analysis aimed at clarifying their effect on sudden death, the magnitude of their benefit according to the cause of heart failure, and whether there is any difference between vasodilating and nonvasodilating agents. METHODS: Randomized, clinical trials were included if they evaluated a beta-adrenergic blocking agent without intrinsic sympathomimetic activity, included a control group receiving placebo or standard treatment, evaluated mortality on an intention-to-treat basis, and lasted at least 8 weeks. RESULTS: Twenty-one trials with 5,849 patients (3,130 receiving beta-blockers) were included. Median length of treatment was 6 months. Most patients had mild or moderate heart failure and were treated with angiotensin-converting enzyme inhibitors, diuretics, and digitalis. The beta-blockers significantly reduced overall mortality, cardiovascular mortality, and mortality due to pump failure and sudden death by 34% to 39%. The decrease in overall mortality in patients with ischemic heart disease (IHD) (30%) was no different from that among patients with non-IHD (26%) (P = .08). The reduction in overall mortality was greater with vasodilating than with nonvasodilating agents (45% vs 27%; P = .007), particularly in patients without IHD (62%), compared with those with IHD (22%; P =.03). CONCLUSIONS: In patients with heart failure, beta-blockers reduce total and cardiovascular mortality at the expense of a decrease in mortality due to pump failure and sudden death. The magnitude of the benefit is similar in patients with IHD and in those with non-IHD. Vasodilating beta-blockers have a greater effect on overall mortality than nonvasodilating agents, particularly in patients with non-IHD.

Adrenergic beta-Antagonists↗
PubMed1982

Effects of 6-hydroxydopamine pretreatment on in vivo femoral arterial responses to vasodilator agents.

Reserpine has been previously shown to generally enhance femoral arterial vasodilator responses as indicated by increased slopes of regression lines relating decreases in resistance produced by injections of vasodilator agents to resistance prior to the injections. We have examined the same parameters in dogs pretreated with 6-hydroxydopamine. In contrast, 6-hydroxydopamine either decreased (nitroglycerin, adenosine) or had no effect (isoproterenol, acetylcholine) on femoral arterial vasodilator responses. In a second set of animals, reserpine was administered after pretreatment with 6-hydroxydopamine, and reserpine again tended to augment responses to vasodilator agents. These data suggest that reserpine's effects on vasodilator responses may be a direct effect on vascular smooth muscle and was not dependent on its effects on sympathetic innervation of the femoral bed. The decreased vasodilator responses to certain agents induced by 6-hydroxydopamine, in contrast, may have been attributable to loss of a presynaptic component of their mechanism(s) of vasodilator action.

Adenosine↗
PubMed1994

Plasma endothelin-1 response to acute hypotension induced by vasodilating agents.

Cyclic GMP (cGMP) dependent vasodilating agents (natriuretic peptides, nitric oxide) inhibit secretion of endothelin-1 (ET-1) in cultured endothelial cells. However, in circulatory conditions associated with acute hypotension, a marked increase in plasma ET-1 has repeatedly been observed. Therefore, after administration of cGMP-dependent agents in hypotensive dose, the net effect of these opposing influences on ET-1 release may shed light on the mechanisms determining circulating levels of this peptide. We have studied the effect of a hypotensive dose of atrial natriuretic peptide (n = 16), 8-Br-cGMP (n = 5), and papaverin (n = 7) on plasma ET-1 in anesthetized dogs. All agents produced marked increases in the peptide level at the end of infusion (178, 280, and 240% of the last preinfusion level, respectively) and a mean arterial blood pressure (MAP) decrease of 19, 18, and 42 mmHg (1 mmHg = 133.3 Pa), respectively. In all three protocols, plasma ET-1 continued to rise when the hypotensive agent was discontinued and remained elevated for 2-3 h postinfusion, even though MAP was normalized. There was a close positive correlation between the maximal increment in plasma ET-1 and the maximal decrease in MAP (r = 0.67, p < 0.001). These results show that acute hypotension due to directly acting vasodilators is a potent stimulus for systemic release of ET-1, even when due to agents known to inhibit ET-1 production in cultured endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗