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

Vasodilators lower the blood pressure by decreasing total peripheral resistance. The hemodynamic changes depend on the mix between arteriolar and venous dilatation. Since the compensatory responses are blunted with sympatholytic agents and diuretics, vasodilators can be applied effectively in the treatment of hypertension. Hydralazine and prazosin are used as step III drugs in combination with beta-adrenergic blockers and diuretics. Only hypertensive patients whose blood pressure is not controlled by standard antihypertensive drugs should receive minoxidil or captopril. Hypertensives receiving minoxidil usually require a loop diuretic such as furosemide, in addition to a beta-blocker. Captopril is usually combined with a thiazide diuretic and frequently also with a beta-adrenergic blocker. For hypertensive emergencies diazoxide must be injected intravenously as a bolus. It is contraindicated in patients with dissecting aortic aneurysm or left ventricular failure. Sodium nitroprusside is effective in most cases of hypertensive crisis and must be administered intravenously under continuous observation.
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PMID:Vasodilators in the treatment of hypertension. 676 Oct 57

Sodium nitroprusside, a direct-acting vasodilator, has been used to treat the hypertension associated with preeclampsia and eclampsia. Fatal cyanide intoxication has been reported during infusion of nitroprusside. We have investigated placental transfer and fetal toxicity of nitroprusside in the acute pregnant ewe model. A maternal intravenous infusion of nitroprusside solution was maintained at a rate sufficient to decrease mean maternal arterial pressure by 20% for 1 hour. Maternal and fetal levels of nitroprusside were in equilibrium at the 20 minute sample. Five of the eight animals exhibited tachyphylaxis to nitroprusside, and their fetuses died in utero with lethal levels of cyanide. No significant changes were observed in uterine blood flow.
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PMID:Fetal toxicity of nitroprusside in the pregnant ewe. 678 82

Although hypertension is the greatest risk factor for stroke, its control with antihypertensive drugs improves survival and decreases the incidence of stroke. If a stroke should occur, careful antihypertensive therapy has not been harmful. Sodium nitroprusside is the initial drug of choice in acute crises.
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PMID:Hypertension and cerebrovascular disease. 690 Nov 85

The hypertension immediately after open heart surgery for coronary heart disease was chosen to evaluate the suitability of computer-controlled infusion sodium nitroprusside, to improve the circulatory state in heart failure by reducing the impedance to the left ventricular ejection. Sodium nitroprusside produced a prompt reduction of MAP to a preset level and a rise in cardiac index from an average of 2.1 +/- 0.3 to 2.4 +/- 0.4 when infused alone and to 3.1 +/- 0.5 1/min m2 (p less than 0.05, + 48%) after volume was infused to maintain LAP at a constant level to eliminate the effects of preload. The rise in cardiac index was associated with marked decrease in systemic vascular resistance from 2260 +/- 530 to 1415 +/- 280 and 1130 +/- 1130 +/- 270 dyns (p less than 0.005, 63%) respectively. The initial values of SVR correlated well with the fall of SVR (r = 0.78). Our results suggest that systemic vascular resistance is a strong indicator of the vascular responsiveness to vasodilation, the computer-controlled infusion of sodium-nitroprusside being suitable for the "titration" of the high systemic vascular resistance.
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PMID:[Hemodynamic effects of computer-guided blood pressure-lowering with nitroprusside sodium during the postoperative phase after aortocoronary bypass operations]. 698 28

Sodium nitroprusside is a potent and ultrafast-acting antihypertensive agent. Limited clinical experience and uncertainty about toxicity have restricted its use in obstetrics. The authors have used nitroprusside concomitantly with hemodynamic monitoring in 4 obstetric patients with severe pregnancy-induced hypertension unresponsive to conventional therapy. The patients with acute congestive heart failure and pulmonary edema responded rapidly and dramatically to nitroprusside. No signs of fetal distress associated with lowering of the arterial pressure were observed, and significant cyanide levels were not detected in a fetal cord blood sample. Nitroprusside should be reserved for refractory hypertensive emergencies in pregnancy. Hemodynamic monitoring is required for adjusting nitroprusside administration and fluid balance. In short-term usage, the authors' experience suggests that maternal and fetal toxicity may not be serious concerns.
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PMID:Use of sodium nitroprusside in complications of gestational hypertension. 712 43

The value of plasma norepinephrine measurement in assessing baroreceptor-mediated changes in sympathetic vasomotor activity was studied in seven healthy normotensive volunteers. Blood pressure was decreased by graded steady-state infusions of sodium nitroprusside (25-100 micrograms/min) and increased by infusions of phenylephrine (25-100 micrograms/min) at rates producing a 10% to 20% change in diastolic blood pressure. Sodium nitroprusside produced significant decreases in diastolic blood pressure (p less than 0.01) and calculated mean arterial blood pressure (p less than 0.005), and increases in heart rate (p less than 0.001) and plasma norepinephrine (p less than 0.001). Phenylephrine administration produced increases in systolic (p less than 0.005), diastolic (p less than 0.005), and mean blood pressure (p less than 0.001). Heart rate (p less than 0.001) and plasma norepinephrine (p less than 0.05) fell. The absolute changes in diastolic and mean pressure and heart rate were not significantly different for the two drugs, but were of opposite sign; however, the increase in plasma norepinephrine during hypotension was greater than the decrease during hypertension (p = 0.02). We conclude that plasma norepinephrine changes appropriately in response to altered blood pressure and that the response is greater to a given fall than to a rise in blood pressure, consistent with known changes in sympathetic vasomotor outflow.
Hypertension
PMID:Plasma norepinephrine in the evaluation of baroreceptor function in humans. 715 32

Sodium nitroprusside (SNP) is frequently used to control hypertension and/or improve systemic blood flow following cardiac operations. Although SNP causes renal vasodilation when infused into isolated kidneys, the reported effects of SNP on renal vascular resistance and blood flow in intact animals and humans have varied. To define the effects of SNP in postoperative cardiac surgical patients, renal clearances and hemodynamics were measured in seven patients within 24 hours of coronary bypass grafting. Studies were delayed until patients were stabilized and had rewarmed following operation. Following baseline measurements (off SNP), SNP infusion was used to lower mean arterial pressure to 85 torr. Pulmonary wedge pressure was maintained by appropriate fluid therapy, and the measurements repeated 1 h later. SNP administration resulted in equivalent decreases in renal (-31 per cent), pulmonic (-29 per cent) and systemic (-33 percent) vascular resistance. Notwithstanding the decrease in arterial pressure (109 +/- 14 to 91 +/- 9 torr, P less than 0.01), renal blood flow increased by 20 per cent (653 +/- 193 to 792 +/- 210 ml . min-1 . 1.73 m-2, P less than 0.02), in direct proportion to the increase in cardiac index (2.5 +/- 0.4 to 3.0 +/- 0.3 1 . min-1 . m-2, P less than 0.01). Thus, in postoperative cardiac surgical patients, SNP administration can be expected to improve renal blood flow, so long as left atrial hypotension is avoided, and the decline in systemic arterial pressure is not excessive. The improvement in renal blood flow achievable with SNP may be critical for patients with severely depressed left ventricular function in whom severe depression of renal blood flow may occur as an antecedent to acute renal failure.
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PMID:The renal effects of sodium nitroprusside in postoperative cardiac surgical patients. 721 28

Sodium nitroprusside (SNP) is known to inhibit platelet aggregation and has been implicated in postoperative hemorrhagic complications. Because it is a useful agent for treating postoperative hypertension and low cardiac output in the cardiac surgical patient, the authors retrospectively reviewed the course of 53 patients undergoing open heart procedures on cardiopulmonary bypass. Twenty-three patients received SNP and 30 did not. There were no differences in baseline hematological or clotting profiles, liver functions, bypass or cross-clamping times or heparin/protamine requirements between the two groups. Analysis revealed no significant differences between the groups in blood product requirements, actual mediastinal drainage, or postoperative measurements of routine clotting parameters. Although biochemical inhibition of platelet aggregation can be demonstrated, the use of SNP in the cardiac surgical patient has no apparent clinical effects which sould detract from its utility in treating hypertension or low cardiac output.
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PMID:Effect of sodium nitroprusside on postoperative blood loss in the cardiac surgical patient. 731 53

Sodium nitroprusside (SNP) is used to control proximal hypertension during cross-clamping of the descending thoracic aorta (XC). To assess the haemodynamic effects of SNP on cardiac output (CO) during XC, 21 pigs were anaesthetized with ketamine and fentanyl. In the control group (n = 11), no vasodilating therapy was given. In the investigation group (SNP group), 2 animals died during the surgical preparation and were excluded, leaving 8 animals in the group (n = 8). In these animals, SNP was infused in order to keep the mean arterial pressure (MAP) at about 100 mm Hg during cross-clamping. In both groups, aorta was cross-clamped for 30 min, and cardiac output (CO) was measured by the thermodilution technique. Following cross-clamping, CO increased 107% in the control group and 96% in the SNP group. There was an increase in heart rate (HR) of 77% in the control group and of 110% in the SNP group, and a reduction in systemic vascular resistance of 41% in the SNP group. Stroke volume (SV) was unchanged in both groups. MAP increased 83% in the control-group. No differences were observed between the two groups regarding central venous pressure or pulmonary artery pressure. Four animals in the SNP group died 5-10 min after release of the aortic clamp. In conclusion, we found equal increase in CO in both groups. The increase in CO was related predominantly to increased HR, whereas SV was largely unaltered. Vasodilation with SNP increased the mortality following clamp removal in this experimental model.
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PMID:Effect of sodium nitroprusside on cardiac output during cross-clamping of the descending thoracic aorta in pigs. 758 4

Attenuated cholinergic vasodilatation has been suggested as an endothelium-related mechanism involved in essential hypertension. We investigated the role of muscarinic (M) receptor subtypes in the forearm resistance vasculature. In eight white men with essential hypertension and eight matched normotensive control subjects (age of both groups, 47 +/- 4 years; mean +/- SEM), we infused the nonselective agonist methacholine in the presence of saline and the antagonists atropine (nonselective), pirenzepine (M1-selective), and AF-DX 116 (M2-selective) into the brachial artery and measured forearm blood flow and forearm vascular resistance using venous occlusion plethysmography. Affinity constants (pKb values) were determined from calculated plasma concentrations of the infused compounds and EC50 values. Sodium nitroprusside was given as an endothelium-independent control, and minimal forearm vascular resistance after 10 minutes of ischemia was used as a marker of structural vascular changes. Hypertensive patients showed higher minimal forearm vascular resistance, indicating structural vascular changes. However, sodium nitro-prusside- and methacholine-induced vasodilatation was similar in both groups, with apparent EC50 values (log moles per liter; mean +/- SEM) of -7.32 +/- 0.13 and -7.51 +/- 0.21 in hypertensive patients and -7.37 +/- 0.13 and -7.45 +/- 0.02 in control subjects, respectively. Atropine, pirenzepine, and AF-DX 116 caused a shift to the right of the concentration-response curve of methacholine, with apparent pKb values of 8.63 +/- 0.08, 6.81 +/- 0.13, and 5.51 +/- 0.29 in hypertensive individuals and 8.62 +/- 0.10, 6.98 +/- 0.08, and 5.49 +/- 0.09 in control subjects, respectively. Again, there were no statistically significant differences in these pharmacological parameters between hypertensive patients and normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Jul
PMID:In vivo characterization of muscarinic receptor subtypes that mediate vasodilatation in patients with essential hypertension. 760 35


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