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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↗
PubMed2003

Relative contribution of vasodilator prostanoids, NO, and KATP channels to human forearm metabolic vasodilation.

Isolated ATP-sensitive K(+) (K(ATP)) channel inhibition with glibenclamide does not alter exercise-induced forearm metabolic vasodilation. Whether forearm metabolic vasodilation would be influenced by K(ATP) channel inhibition in the setting of impaired nitric oxide (NO)- and prostanoid-mediated vasodilation is unknown. Thirty-seven healthy subjects were recruited. Forearm blood flow (FBF) was assessed using venous occlusion plethysmography, and functional hyperemic blood flow (FHBF) was induced by isotonic wrist exercise. Infusion of N(G)-monomethyl-l-arginine (l-NMMA), aspirin, or the combination reduced resting FBF compared with vehicle (P < 0.05). Addition of glibenclamide to l-NMMA, aspirin, or the combination did not further reduce resting FBF. l-NMMA decreased peak FHBF by 26%, and volume was restored after 5 min (P < 0.05). Aspirin reduced peak FHBF by 13%, and volume repaid after 5 min (P < 0.05). Coinfusion of l-NMMA and aspirin reduced peak FHBF by 21% (P < 0.01), and volume was restored after 5 min (P < 0.05). Addition of glibenclamide to l-NMMA and aspirin did not further decrease FHBF. Vascular K(ATP) channel blockade with glibenclamide does not affect resting FBF or FHBF in the setting of NO and vasodilator prostanoid inhibition.

ATP-Binding Cassette Transporters↗
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↗
PubMed2001

L-arginine improves post-ischemic vasodilation in coronary heart disease patients taking vasodilating drugs.

BACKGROUND: The hypothesis that intravenous L-arginine infusion improves the vasodilatory response to ischemia in the resistance vessels of human lower limbs in relatively young coronary heart disease patients taking vasodilating drugs was tested. METHODS: Twenty patients with onset of symptoms of coronary artery disease before age 50, operated for aortocoronary bypass and taking vasodilating drugs, were compared with 20 control subjects of comparable age and gender; neither group included heavy smokers (>10 cigarettes/day). Blood flow in the lower limbs was measured noninvasively with strain-gauge plethysmography, both at rest and during a reactive hyperemia test. Intravenous infusion of L-arginine was performed in nine coronary heart disease patients and in nine control subjects. RESULTS: Resting blood flow to the lower limbs was 2.3 mL/min/100 mL in control subjects vs 3.4 mL/min/100 mL in patients (difference not statistically significant). Peak blood flow measured after a 3-minute arterial occlusion was 24.0 mL/min/100 mL in control subjects vs 20.3 mL/min/100 mL in coronary heart disease patients (P<0.05). Peripheral minimal vascular resistances were 4.28 and 5.46 peripheral resistances units (p.r.u.) in control subjects and patients, respectively (P<0.05). Intravenous infusion of L-arginine was followed by increased resting blood flow in cases and controls (P=0.009), with a parallel reduction in peripheral resting vascular resistances (P=0.009). Coronary heart disease patients showed increased peak blood flow (P=0.04) and reduced minimal vascular resistances (P=0.02), whereas no statistically significant changes in these parameters were detectable in control subjects. Intravenous glucose infusion, leading to increased serum insulin concentration, did not modify any hemodynamic parameter. CONCLUSIONS: Hemodynamic responses in the skeletal muscle are impaired during a reactive hyperemia test in relatively young coronary heart disease patients taking vasodilating drugs. Intravenous L-arginine infusion corrects the impaired vasodilatory response of the lower limbs to an acute increase in flow following a cuff thigh occlusion.

Adult↗
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↗
PubMed1993

Impaired acetylcholine-mediated vasodilation in patients with congestive heart failure. Role of endothelium-derived vasodilating and vasoconstricting factors.

BACKGROUND: The vasodilatory response to intra-arterial administration of acetylcholine is reduced in patients with congestive heart failure compared with that of normal subjects. The reduced response to acetylcholine may be related to decreased endothelial release of nitric oxide, interaction with peripheral alpha-adrenergic transmission, or production of cyclooxygenase-dependent vasoconstricting substances. The extent to which each of these mechanisms contributes to the reduced vasodilatory response to acetylcholine in patients with congestive heart failure is not known. METHODS AND RESULTS: Thirty-one patients with congestive heart failure (New York Heart Association functional class II-III) and five age-matched normal subjects were studied. Regional vascular responses in the forearm to infusions of acetylcholine, an endothelium-dependent vasodilator (10(-7) to 10(-5) mol/L) and nitroglycerin, an endothelium-independent vasodilator (10(-6) mol/L) in the brachial artery were determined with venous occlusion plethysmography before and after regional alpha-adrenergic blockade with intra-arterial phentolamine (25 micrograms/min) and systemic cyclooxygenase with oral indomethacin (50 mg). Administration of phentolamine significantly increased resting baseline forearm blood flow in 11 patients with congestive heart failure (2.9 +/- 0.4 to 5.4 +/- 0.8 mL.min-1.100 mL-1) and normal subjects (4.6 +/- 0.3 to 11.3 +/- 2.1 mL.min-1.100 mL-1). Before administration of phentolamine, intra-arterial infusions of acetylcholine 10(-7), 10(-6), and 10(-5) mol/L increased forearm blood flow to 4.0 +/- 1.0, 6.0 +/- 1.7, and 16.1 +/- 4.0 mL.min-1.100 mL-1, respectively, in patients with congestive heart failure and to 14.7 +/- 6.2, 20.2 +/- 4.7, and 38.7 +/- 7.9 mL.min-1.100 mL-1, respectively, in normal subjects. After administration of phentolamine, the vasodilatory responses to intra-arterial infusions of acetylcholine and nitroglycerin did not change in either patients or normal subjects. Administration of indomethacin did not alter resting forearm blood flow in 15 patients with congestive heart failure (2.7 +/- 0.4 to 2.7 +/- 0.4 mL.min-1.100 mL-1) or normal subjects (4.6 +/- 0.3 to 5.4 +/- 0.8 mL.min-1.100 mL-1). Administration of indomethacin significantly increased the vasodilatory response to infusion of acetylcholine by an average of 39% in patients with congestive heart failure but did not change the vasodilatory response to acetylcholine in normal subjects. In patients with congestive heart failure, baseline forearm blood flow and the vasodilatory responses to intra-arterial infusions of acetylcholine and nitroglycerin were significantly less than those of normal subjects both before and after administration of phentolamine and indomethacin. CONCLUSIONS: The reduced vasodilatory response to intra-arterial infusion of acetylcholine in patients with congestive heart failure probably results from several coexistent abnormalities in peripheral vascular function, including abnormal production of cyclooxygenase-dependent vasoconstricting factor, impaired endothelial release of nitric oxide, and decreased vascular smooth muscle responsiveness to cyclic GMP-mediated vasodilation.

Acetylcholine↗
PubMedDate not supplied

[Comparative vasodilator action of 5 vasodilators: dihydroergotoxine, nicergoline, papaverine, naftidrofuryl and buflomedil on the femoral artery of the dog].

1. Papaverine (PAP), Naftidrofuryl (NAF), Buflomedil (BUF), Nicergoline (NIC) and Dihydroergotoxine (DIT) were injected in the dog iliac artery at increasing doses (25, 100, 400, 1600 micrograms . kg-1) successively at 10 minutes intervals and the femoral blood flow was measured with an electromagnetic flowmeter. The same volume of saline was injected in the contralateral iliac artery. Heart rate and radial artery pressure were measured and the femoral resistances computed. Noradrenaline (2 microgram . kg-1) was injected before and after the highest dose of vasodilators. 2. The three muscular vasodilators (PAP, BUF, NAF) had an immediate, powerful, dose-dependent but short lasting effect since only after 1600 microgram . kg-1 of PAP, there was still a significant vasodilator effect after the tenth minute. Little or no effect was observed on systemic blood pressure except for the higher doses of these compounds which produced a slight decrease accompanied by a simultaneous tachycardia. 3. The two ergot derivatives NIC and DHT caused a moderate but much longer acting decrease of femoral resistance although 100 micrograms . kg-1 DHT also caused an increase of the femoral resistance. This biphasic effect has been already described on other experimental models. The higher doses of these compounds decreased systemic blood pressure and produced a slight bradycardia as already reported (Boismare and Lefrancois, 1978; Huchet et al., 1981; Moore et al., 1981). The pressor effect of noradrenaline was reversed by NIC and DHT, confirming their alpha adrenoceptor blocking properties.

Animals↗
PubMed1983

In search of mediators of skin vasodilation induced by transcutaneous nerve stimulation: I. Failure to block the response by antagonists of endogenous vasodilators.

Low-frequency transcutaneous nerve stimulation (TNS) produces marked and widespread increases in skin temperature in ischaemic limbs of patients with Raynaud's disease and diabetic polyneuropathy. The prolonged time course of the temperature rise, which is due to increased cutaneous microcirculation, indicates the involvement of a long-lasting neurohumoral substance or metabolite. The vascular response is insensitive to conventional low doses of naloxone (Kaada, 1982a). In the present study the possible release of known endogenous vasodilators, all operating through the sympathetic nerves (Fig. 1, Nos 2-8), have been tested in patients by employing selective pharmacological antagonists or inhibitors to see if the stimulation-induced vasodilation could be blocked. The response was not antagonised either by beta-adrenergic, cholinergic, histaminergic, purinergic, or dopaminergic antagonists or by inhibitors of prostaglandins or plasma kinins.

Adult↗
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↗
PubMedDate not supplied

Coronary vasodilator compared to cardiac effects of PY 108-068, a new dihydropyridine vasodilator, on isolated, blood-perfused dog-heart preparations.

We evaluated coronary vasodilator and cardiac effects of PY 108-068 on isolated, blood-perfused sinoatrial (SA) node, atrioventricular (AV) node, and papillary muscle preparations of dogs. PY 108-068 was administered intra-arterially (i.a.). PY 108-068 increased (coronary) blood flow in all preparations. In SA node preparations, the drug produced a decrease in sinus rate and, in large doses, atrial standstill. In AV node preparations, the drug produced an increase in AV conduction time. Large doses caused second- or third-degree AV block, but only when injected into the artery supplying the AV node. The doses producing a 15% (nearly half maximum) decrease in sinus rate or a 15% (nearly half maximum) increase in AV conduction time were two to three times the doses that doubled coronary blood flow. In paced papillary muscle preparations, the drug produced a decrease in the force of contraction. However, the dose required to reduce the force of contraction of the papillary muscle by 50% was about 30 times the dose that doubled coronary blood flow. The drug was entirely ineffective on rate of ventricular automaticity. We conclude that PY 108-068 is not likely to produce reflex tachycardia when administered systemically in coronary vasodilator doses.

Animals↗
PubMed2004

Vasodilator stress induces infrequent wall thickening abnormalities compared to perfusion defects in mild-to-moderate coronary artery disease: implications for the choice of imaging modality with vasodilator stress.

BACKGROUND: Experimental evidence suggests that although vasodilator stress agents consistently induce regional flow disparity between stenosed and normal coronary vascular beds, the occurrence of functional myocardial ischemia is infrequent, especially in mild-to-moderate coronary artery stenosis. Thus, it is hypothesized that dipyridamole infusion, even at high doses, will result in a disproportionately higher frequency of perfusion defects compared to regional wall thickening abnormalities. METHODS: We performed simultaneous high-dose (0.84 mg/kg) dipyridamole stress echocardiography (Echo) and Tc-99m sestamibi SPECT (MIBI, methoxyisobutyl isonitrile) in 46 patients with coronary artery diameter stenosis >50% and < o =90% in one or two epicardial coronary arteries, and no previous myocardial infarction. RESULTS: Of a total of 828 segments, MIBI showed 97 reversible defects while Echo showed only 23 reversible wall thickening abnormalities. Of the 97 segments with reversible MIBI defects, only 13 (13%) showed simultaneous reversible wall thickening abnormalities during dipyridamole infusion. There were 24 patients with MIBI defects, of whom 10 (41%) showed a corresponding wall thickening abnormality. The sensitivity of MIBI and Echo for the detection of coronary artery disease was 52% and 21%, respectively (P = 0.001). CONCLUSION: This suggests that vasodilator stress is not optimally suited for use with techniques that use regional wall thickening abnormality as a marker of ischemia for the diagnosis of coronary artery disease.

Aged↗
PubMed1997

Effect of the calcium antagonist felodipine as supplementary vasodilator therapy in patients with chronic heart failure treated with enalapril: V-HeFT III. Vasodilator-Heart Failure Trial (V-HeFT) Study Group.

BACKGROUND: Despite therapy with diuretics, ACE inhibitors and digoxin morbidity and mortality in heart failure remain high and might respond favorably to an additional vasodilator. METHODS AND RESULTS: Male patients (n=450) with chronic heart failure (cardiac dysfunction and impaired exercise performance) on optimal current therapy (97% enalapril, 89% diuretics) were randomly assigned to double-blind treatment with felodipine extended release (5 mg BID) or placebo for 3 to 39 months (average, 18 months). Felodipine significantly reduced blood pressure and, at 3 months, increased ejection fraction (2.1% versus -0.1% units in the placebo group, P=.001) and reduced plasma atrial natriuretic peptide levels (-2.9 versus 26.9 pg/mL in the placebo group, P=.01) but did not improve exercise tolerance, quality of life, or the need for hospitalization. During long-term follow-up, the favorable effects on ejection fraction and atrial peptide did not persist, but felodipine prevented worsening exercise tolerance and quality of life. In the felodipine and placebo groups, mortality (13.8% versus 12.8%, respectively) and hospitalization (43% versus 42%) rates were similar, and a higher incidence of peripheral edema was the only apparent side effect of felodipine therapy. CONCLUSIONS: Felodipine exerts a well-tolerated additional sustained vasodilator effect in patients with heart failure treated with enalapril, but the only possible long-term benefit was a trend for better exercise tolerance and less depression of quality of life in the second year of treatment. The drug appears to be safe but not clearly efficacious in patients with heart failure.

Adult↗
PubMed2001

Preferential acetazolamide-induced vasodilation based on vessel size and organ: confirmation of peripheral vasodilation with use of colored microspheres.

When carbonic anhydrase activity decreases, the regional blood flow (rBF) in organs increases as hypercapnia develops. However, the effects of acetazolamide (AZ)-induced vasodilation have not been estimated with respect to vessel size and organs. The aim of this study was to determine the diameter of the capillaries in various organs that respond to inhibition of carbonic anhydrase activity by AZ. White rabbits were anesthetized with urethane and ketamine and infused with AZ. While the systolic blood pressure (SBP), pH, hemoglobin concentration, and base excess did not change, the partial pressure of arterial oxygen (PaO2) increased significantly and the partial pressure of arterial carbon dioxide (PaCO2) decreased significantly with AZ. The rBF was calculated by using 3 different sizes (15, 25, and 50 microm) of colored microspheres (CM). The rBF measured with 15 microm CM in the brain, kidneys, and liver increased in response to AZ, and the rBF in these organs was different with the different sizes of CM. However, the rBF calculated by using the different sizes of CM in the stomach and abdominal muscle did not change after the administration of AZ. The AZ-induced vasodilation occurred in all sizes of vessels in the liver, in the small and medium-sized vessels in kidneys, and in the larger capillaries in the brain.

Abdominal Muscles↗
PubMed2000

Vasodilator responses to ATP and UTP are not dependent on nitric oxide release, K+(ATP) channel activation, or the release of vasodilator prostaglandins in the hindlimb vascular bed of the cat.

The effects of the purinergic agonists, ATP, ATPgammaS, UTP, and 2-Met-Thio AP, were investigated in the hindlimb vascular bed of the cat. Under constant-flow conditions, injections of the purinergic agonists into the perfusion circuit elicited dose-related decreases in perfusion pressure. The order of potency was 2-Met-Thio ATP > ATPgammaS > ATP > UTP. In contrast, injections of GTPgammaS, cAMP, UDP, and UMP had no effect. Vasodilator responses to ATP, ATPgammaS, UTP, and 2-Met-Thio ATP were increased in duration by the cAMP phosphodiesterase inhibitor rolipram, whereas the cGMP phosphodiesterase inhibitor zaprinast had no effect. Responses to the purinergic agonists were not altered by nitric oxide synthase inhibitors, K+(ATP) channel antagonists, cyclooxygenase inhibitors, or agents that interfere with the actions of the adrenergic nervous system. These data suggest that ATP, ATPgammaS, UTP, and 2-Met-Thio ATP dilate the hindlimb vascular bed by a direct cAMP-dependent mechanism, and that the release of nitric oxide, vasodilator prostaglandins, K+(ATP) channel opening, or an inhibitory effect on the adrenergic nervous system play little, if any, role in mediating or modulating responses to the purinergic agonists in the hindlimb circulation of the cat.

Adenosine Triphosphate↗
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↗
PubMed1999

Racial differences in response to therapy for heart failure: analysis of the vasodilator-heart failure trials. Vasodilator-Heart Failure Trial Study Group.

BACKGROUND: Heart failure in blacks has been associated with a poorer prognosis than in whites. In such diseases as hypertension, blacks show pathophysiological differences and respond differently to some therapies than whites. The aim of this study is to evaluate the clinical characteristics and response to therapy of black compared with white patients with heart failure. METHODS AND RESULTS: In the first Vasodilator-Heart Failure Trial (V-HeFT I), 180 black male patients were compared with 450 white male patients for baseline characteristics, prognosis, and response to therapy. In V-HeFT II, the same comparisons were made for 215 black and 574 white male patients, including an analysis stratified by the presence or absence of a history of hypertension. In both trials, black patients had a lower incidence of coronary artery disease, greater incidence of previous hypertension, and a greater cardiothoracic ratio (P < .05) than white patients. In V-HeFT II, plasma norepinephrine levels were significantly less in blacks; plasma renin activity was less only in blacks with a history of hypertension. Overall mortality or hospitalization for congestive heart failure did not differ between blacks and whites in the placebo group in V-HeFT I. However, the mortality of black patients receiving hydralazine plus isosorbide dinitrate (H-I) was reduced (P = .04) in V-HeFT I, whereas white patients showed no difference from placebo. In V-HeFT II, only white patients showed a mortality reduction from enalapril therapy compared with H-I therapy (P = .02). Whites also showed evidence of greater blood pressure reduction and enhanced regression of cardiac size in response to enalapril. When stratified by history of hypertension in V-HeFT II, only whites with a history of hypertension, who had greater renin levels, showed significant mortality reduction with enalapril compared with H-I therapy. Hospitalization rates did not differ between treatment groups in either study. CONCLUSION: Whites and blacks showed differences in cause, neurohormonal stimulation, and pharmacological response in heart failure. This retrospective analysis suggests angiotensin-converting enzyme inhibitors are particularly effective in whites, and the H-I combination can be equally effective in blacks. Prospective trials involving large numbers of black patients are needed to further clarify their response to therapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

A new inorganic vasodilator, trans-[Ru(NO)(NH(3))(4)(POEt)(3)](PF(6))(3): hypotensive effect of endothelium-dependent and -independent vasodilators in different hypertensive animals models.

The hypotensive effect of RuNO was investigated in acute and chronic hypertensive rats, as well as in normotensive rats. Acute hypertension rats were used with 30% increase on basal BP (phenylephrine, angiotensin II (Ang II), N(G)-nitro-L-arginine methyl ester (L-NAME), and adult spontaneously hypertensive rats (SHR) (basal BP 168 +/- 3 mm Hg) were used as models for chronic hypertension. Rats were implanted with catheters (iv/ia) for BP measurements and for in bolus administration of RuNO, sodium nitroprusside (SNP), and acetylcholine (Ach) (10, 20, 40 nmol/kg, iv). The principal findings of this study were: (i) The hypotensive response to RuNO was 150% higher in acutely (phenylephrine and Ang II) and chronically (SHR) hypertensive rats than in normotensive rats, except in the case of L-NAME-induced hypertension (deltaMAP = 10 +/- 1.4 mm Hg). Chronic SHR showed 60% increase (deltaMAP = 19 +/- 0.8 mm Hg) in the effect compared to normotensive rats. (ii) The hypotensive response to SNP was lower (60%) in hypertensive rats than in normotensive rats, when compared to RuNO. However, the responses were similar in L-NAME-induced hypertension (deltaMAP = 30 +/- 2 mm Hg). (iii) The vasodilator response to Ach was increased in rats with Ang II-induced hypertension (deltaMAP = 53 +/- 1 mm Hg) and in SHR (deltaMAP = 67 +/- 3 mm Hg). RuNO response was more potent than SNP in hypertensive models and the increment in relation to normotensive was observed in the phenylephrine- and L-NAME-treated rats. This response could be correlated to the different endothelial dysfunction present in each model.

Acetylcholine↗