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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brainstem catecholaminergic neurons have been implicated as mediating adaptive autonomic and neuroendocrine responses to cardiovascular challenges. To clarify the nature of this involvement, immuno- and hybridization histochemical methods were used to follow c-fos expression in these neurons in response to acute stimuli that differentially affect blood pressure and volume. From low basal levels, hypotensive hemorrhage (15%) provoked a progressive increase in the number and distribution of Fos-immunoreactive (ir) nuclei in the nucleus of the solitary tract (NTS), the A1 and C1 cell groups of the ventrolateral medulla, and in the pontine A5, locus coeruleus, and lateral parabrachial cell groups peaking at 2.0-2.5 hours after the challenge. Fos-ir ventrolateral medullary neurons, subsets of which were identified as projecting to the paraventricular hypothalamic nucleus or spinal cord, were predominantly aminergic, whereas most of those in the NTS were not. Infusion of an angiotensin II antagonist blunted hemorrhage-induced Fos expression in the area postrema, and attenuated that seen elsewhere in the medulla and pons. Nitroprusside-induced isovolemic hypotension yielded a pattern of c-fos induction similar to that seen following hemorrhage, except in the area postrema and the A1 cell group, where the response was muted or lacking. Phenylephrine-induced hypertension stimulated a restricted pattern of c-fos expression, largely limited to induced hypertension stimulated a restricted pattern of c-fos expression, largely limited to non-aminergic neurons, whose distribution in the NTS conformed to the termination patterns of primary baroreceptor afferents, and in the ventrolateral medulla overlapped in part with those of vagal cardiomotor and depressor neurons. These findings underscore the importance of brainstem catecholaminergic neurons in effecting integrated homeostatic responses to cardiovascular challenges and their ability to responding strategically to specific modalities of cardiovascular information. They also foster testable predictions as to effector neuron populations that might be recruited to respond to perturbations in individual circulatory parameters.
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PMID:Spatially and temporally differentiated patterns of c-fos expression in brainstem catecholaminergic cell groups induced by cardiovascular challenges in the rat. 784 57

Thirty-three patients with severe systemic hypertension defined as a diastolic blood pressure (DBP) > or = 120 mm Hg were randomized in a single-blind fashion to be treated with either intravenous fenoldopam mesylate (FNP) or sodium nitroprusside (NTP). Fenoldopam mesylate and NTP infusion rates began at 0.1 microgram/kg/minute and 0.5 microgram/kg/minute, respectively and were titrated to achieve a goal DBP of between 95 and 110 mm Hg; or a reduction of at least 40 mm Hg if the baseline DBP was > 150 mm Hg. Fenoldopam mesylate (n = 15) reduced blood pressure from 217/145 +/- 6/5 to 187/112 +/- 6/3 mm Hg (P < .001) at an average infusion rate of 0.5 +/- 0.1 microgram/kg/minute. The average time to achieve goal DBP with FNP was 1.5 +/- 1.4 hours. Nitroprusside (n = 18) reduced blood pressure from 210/136 +/- 5/2 to 172/103 +/- 6/2 mm Hg (P < .001) at an average infusion rate of 1.2 +/- .24 micrograms/kg/minute. Nitroprusside response time averaged 2 +/- 2.5 hours. There was no significant difference between the magnitude of effect seen with either FNP or NTP; nor was there any difference observed in the adverse effect rates of the two agents. Fenoldopam mesylate and NTP demonstrate similar overall efficacy in the treatment of severe systemic hypertension.
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PMID:Fenoldopam mesylate versus sodium nitroprusside in the acute management of severe systemic hypertension. 810 27

Studies in vitro and in vivo have implicated nitric oxide in the control of renin secretion. In the present study, the effect of inhibition of nitric oxide synthesis with NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) on the renin secretory response to beta-adrenergic stimulation was investigated in conscious, chronically prepared rabbits. Intravenous infusion of isoproterenol at 0.02 microgram.kg-1 x min-1 for 30 minutes increased mean arterial pressure by 5 mm Hg (P < .05), heart rate by 51 beats per minute (P < .001), and plasma renin activity by 56% (P < .001). Intravenous infusion of L-NAME at 0.5 mg.kg-1 x min-1 increased mean arterial pressure by 6 mm Hg (P < .01) and decreased heart rate by 15 beats per minute (P < .01) and plasma renin activity by 31% (P < .05). L-NAME reduced the heart rate response to isoproterenol by 50% and inhibited the renin response. Infusion of isoproterenol at 0.05 microgram.kg-1 x min-1 did not change blood pressure but increased heart rate by 62 beats per minute (P < .001) and plasma renin activity by 283% (P < .001). Treatment with L-NAME again suppressed the heart rate response to isoproterenol and inhibited the renin response. Intravenous infusion of the nitric oxide donor nitroprusside at 2 micrograms.kg-1.min-1 in the presence of L-NAME decreased mean arterial pressure by 7 mm Hg (P < .05), increased heart rate by 14 beats per minute (P < .05), but did not change plasma renin activity. Nitroprusside fully restored the heart rate response to isoproterenol and partially restored the renin response.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1994 Jan
PMID:Role of nitric oxide in the renin and heart rate responses to beta-adrenergic stimulation. 828 75

Perioperative hypertension is primarily due to increased systemic vascular resistance (SVR). Therefore, the major therapeutic approaches are directed at reducing vasoconstriction, using drugs that increase cyclic nucleotides or block calcium entry into vascular smooth muscle. Nitroprusside and other nitric oxide-derived vasodilators affect both the resistance vessels and the vascular capacitance bed. Antihypertensive drugs that affect venous return can have unpredictable effects on blood pressure and calculated SVR. The new intravenous dihydropyridine calcium antagonists have arterial vasodilating actions and are especially promising as new therapeutic approaches for perioperative hypertension. Following coronary bypass-grafting, patients have undergone direct mechanical manipulation of their native grafts, coronary arteries, and internal mammary artery, creating a potential risk for coronary or internal mammary spasm. Calcium antagonists may be an important therapy for perioperative hypertension in such patients. Experimental models have demonstrated that calcium antagonists can attenuate the production of inflammatory mediators and thereby reduce cellular damage following reperfusion. These potential anti-inflammatory drugs may prove to offer additional benefits in the therapy of perioperative hypertension. The potential anti-inflammatory and cytoprotective effects of calcium antagonists may make them the ideal agents for the treatment of acute perioperative hypertension.
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PMID:The ideal agent for perioperative hypertension and potential cytoprotective effects. 848 May 2

Hypertensive crisis is a rare condition with increased blood pressure and evidence of new or progressive severe end-organ damage. The patients should be admitted to hospital, and the blood pressure reduced gradually. Blood pressure should not be normalized, but a reduction in mean arterial pressure of 20-25% or to a diastolic blood pressure > 100-110 mmHg should be achieved. Patients at particular risk for further complications are elderly, patients with hypovolaemia, renal insufficiency, ischaemic heart disease and patients with neurological deficits. The ideal antihypertensive drug for any form of hypertensive crisis does not exist. If the patient can cooperate with oral treatment, nifedipine may be used, usually administered as capsules of 10 mg orally, producing a rapid and safe reduction in blood pressure of 25% within 10-15 minutes with a maximal action after 30-60 minutes. The dose may be repeated after 30 minutes in case of insufficient blood pressure response. Hypotension is rare. Nifedipine in combination with nitroglycerine is of special benefit in hypertensive pulmonary oedema. In cases of treatment failure or if the patient cannot cooperate with oral treatment, the choice of drug lies between labetalol and sodium nitroprusside. Nitroprusside is administered as continuous intravenous infusion, the drug is safe to use and is recommended in conditions where reduction of blood pressure must be performed with extreme caution such as in cases of cerebral infarction and intracranial hemorrhage. Infusion of nitroprusside for more than 48-72 hours is inexpedient because the metabolites of nitroprusside need monitoring as well. Parenteral drug therapy with labetalol is more simple than treatment with nitroprusside, but at the same time somewhat more difficult to titrate. Nitroglycerine is very suitable in moderate hypertension and ischaemic heart disease, but in severe hypertension with heart disease nitroprusside is the treatment of choice. Loop diuretics should not be used as first-line drugs, but only in conditions with evidence of volume-overload. Patients with hypertensive crisis most often show volume depletion which is aggravated by loop diuretics, therefore they should not be used routinely. When the blood pressure has been stabilized, an oral antihypertensive drug should be started concomitantly to a gradual reduction of the initial parenteral drug therapy.
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PMID:[Hypertensive crises. 2. Treatment]. 875 95

Nitroglycerin and the long-acting nitrates have been used in cardiovascular medicine for >100 years. Nitrates are widely utilized for the various anginal syndromes and are also used in congestive heart failure and patients with left ventricular dysfunction. The potential mechanisms for relief of myocardial ischemia with nitrates are multiple. The nitrovasodilators are a related group of drugs that result in the formation of nitric oxide (NO) within vascular smooth muscle cells. NO stimulates the enzyme guanylate cyclase, which results in increases in cyclic guanosine monophosphate and vasodilation. In the presence of atherosclerosis, endothelial dysfunction is ubiquitous and associated with decreased NO availability, probably due to increased destruction of NO by free radical anions. Nitrovasodilators, including the nitrates, supply exogenous NO to the vascular wall and improve the vasodilator state. When nitrates are administered, endothelial-dependent stimuli cause relaxation rather than constriction in the setting of endothelial dysfunction. Nitrates also have antiplatelet effects, and recent evidence confirms that these drugs decrease platelet aggregation and thrombosis formation. This may play an important role in the therapy of acute unstable myocardial ischemia, including unstable angina and myocardial infarction. Nitrate hemodynamic effects have been long known. They are primarily modulated through a decrease in myocardial work that results from smaller cardiac chambers operating with lower systolic and diastolic pressures. These changes are caused by a redistribution of the circulating blood volume away from the heart to the venous capacitance system, with a fall in venous return to the heart. The afterload or arterial effects of nitrates are also useful in decreasing myocardial oxygen consumption. Considerable evidence confirms a variety of mechanisms whereby nitrates increase coronary blood flow, including epicardial coronary artery dilation, stenosis enlargement, enhanced collateral size and flow, improvement of endothelial dysfunction, and prevention or reversal of coronary artery vasoconstriction. These effects help increase nutrient coronary blood flow to zones of myocardial ischemia. Recent data with the nitroglycerin patch confirm that myocardial ischemia is decreased after nitrate administration. Nitroprusside, another nitrovasodilator, is a commonly used intravenous agent for lowering arterial pressure and left ventricular filling pressure. This drug is highly effective for the treatment of acute or severe hypertension and congestive heart failure. However, there are data suggesting that nitroprusside may be deleterious in the presence of acute myocardial ischemia, perhaps by shunting blood away from zones of jeopardized myocardial blood flow. Therefore, nitroprusside cannot be recommended to treat myocardial ischemia; intravenous nitroglycerin should be used in this context.
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PMID:Beneficial actions of nitrates in cardiovascular disease. 863 24

Neurons immunoreactive for Fos, the protein product of the immediate early gene c-fos, have been compared in the rostral ventral medulla and spinal cord of conscious normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) after baroreceptor unloading. Hypotension induced by a 60-minute intravenous infusion of sodium nitroprusside reduced baroreceptor activity; controls received intravenous saline. In WKY, 474 +/- 56 (n=6) Fos-positive neurons were identified in the rostral ventral medulla after nitroprusside infusion, a fivefold increase from controls; 50% of the tyrosine hydroxylase-containing neurons in the rostral ventral medulla were activated by this hypotension. Sympathetic preganglionic neurons, mainly sympathoadrenal neurons, were Fos positive after nitroprusside, but Fos-positive sympathetic preganglionic neurons were not observed in control WKY. In SHR, Fos immunoreactivity in the rostral ventral medulla was elevated in the control group compared with the WKY controls (236 +/- 31 and 93 +/- 15, respectively, n=6 for both). Nitroprusside hypotension did not further increase Fos immunoreactivity in the rostral ventral medulla, although the number of Fos-positive spinal sympathetic neurons increased. Our results have identified different neuronal activities between WKY and SHR in sites that are critical to sympathetic outflow. In WKY, nitroprusside effects are consistent with an activation of rostral ventral medulla neurons, including bulbospinal neurons, that are normally inhibited by baroreceptor activity. In SHR, basal nerve activity is increased, so even at rest, rostral ventral medulla neurons and sympathetic preganglionic neurons, mainly sympathoadrenal neurons, are Fos immunoreactive. These activated neurons are likely to contribute to the elevated blood pressure in this rat strain.
Hypertension 1996 Mar
PMID:Altered c-fos in rostral medulla and spinal cord of spontaneously hypertensive rats. 869 50

Consecutive catheterizations in 512 patients with mitral valve disease revealed 85 cases of mitral stenosis with systolic pulmonary artery pressures equal to or in excess of 100 mm Hg. Forty-four patients (51.8%) were in New York Heart Association functional Class IV; 30 (35.3%) were in Class III; and 11 (12.9%) were in Class II. Symptoms related to pulmonary capillary hypertension were prominent in 48 patients (56.5%) while the remaining patients showed signs of low cardiac output syndrome. Forty patients underwent surgery: mitral commissurotomy was performed in 26 patients; mitral valve replacement in 10 patients, and double valve replacement in four patients. Nitroprusside was infused into the pulmonary artery in six patients with severe perioperative low cardiac output; four of these patients survived. The overall operative mortality was 15% (six patients). Good long-term results were achieved in 30 cases.
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PMID:Mitral stenosis with severe pulmonary hypertension. 1522 32

Male Sprague-Dawley rats underwent sinoaortic denervation (SAD) or sham operation. We examined changes in the release rates of GABA, glutamate and arginine in the locus coeruleus (LC) elicited by experimental blood pressure increases (i.v. noradrenaline infusion for 3 min, 4 microg kg(-1)min(-1)) or decreases (i.v. sodium nitroprusside infusion for 3 min, 150 microg kg(-1)min(-1)). The release of the neurotransmitters was monitored by the push-pull superfusion technique. Mean blood pressure did not differ between sham-operated and SAD rats but blood pressure lability was greatly enhanced in SAD rats and accompanied by increased basal release of glutamate in the LC. GABA release was not affected. A rise in blood pressure induced by noradrenaline enhanced GABA release in the LC of sham-operated rats. This effect was abolished by SAD. Glutamate release did not respond to hypertension either in SAD or in sham-operated rats. Nitroprusside led to a fall in blood pressure which was more pronounced and lasted longer in SAD than in sham-operated rats. In SAD rats, glutamate release was enhanced by nitroprusside. The depressor response had no effect on glutamate release in sham-operated rats. GABA release did not respond to this stimulus in either SAD or sham-operated rats. SAD and blood pressure changes did not influence the release rate of arginine. In conclusion, experimental hypertension increases GABAergic activity in the LC by stimulating peripheral baroreceptors. In SAD rats, augmented blood pressure lability seems to be at least partly due to elevated glutamate outflow within the LC.
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PMID:Sinoaortic denervation abolishes blood pressure-induced GABA release in the locus coeruleus of conscious rats. 1623 53

Congenital aortic stenosis is a relatively common cardiac anomaly encountered in approximately 5% of all children with heart disease. The Ross procedure is increasingly used for replacement of the aortic valve in children. We report a 12-year-old boy who was born with congenital aortic stenosis secondary to a bicommissural aortic valve. The patient underwent open valvotomy in infancy and aortic valvuloplasty 2 years later. Residual/recurrent stenosis prompted referral for aortic valve replacement, and he underwent an autologous Ross procedure, in which the aortic root was replaced with a pulmonary autograft and the repaired aortic valve was used to restore right ventricular-to-pulmonary artery continuity. The postoperative course was unremarkable. Nitroprusside, esmolol, and labetolol were used to control postoperative hypertension. He was discharged 4 days after surgery on oral furosemide and aspirin, and he has had no cardiovascular symptoms during follow-up. Recent echocardiography demonstrated mild right ventricular outflow tract obstruction with a peak velocity of 3.6 m/sec, with a gradient of 42 mmHg and moderate pulmonary insufficiency. There was no left ventricular outlet tract obstruction or aortic insufficiency.
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PMID:Autologous Ross operation for congenital aortic stenosis. 1703 18


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