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

The effect of microinjection into the nucleus tractus solitarii (NTS) of angiotensin II (Ang II) on baroreceptor control of heart rate (HR) in conscious, freely moving rats was evaluated with a new method of long-term cannulation of the dorsal brainstem areas. Reflex changes in HR were produced by intravenous bolus injections of either phenylephrine or sodium nitroprusside (0.2-25.6 micrograms/kg) both after saline and after unilateral microinjection of Ang II into the NTS (24 ng, 0.2 microliter) and compared with those produced after administration of Ang II into the fourth ventricle (24 ng, 0.2 microliter) or intravenously (1-2 ng/kg/min). Baseline levels of mean arterial pressure (MAP) and HR were not affected by the route of Ang II application but reflex bradycardia during MAP increase was significantly attenuated after injections of Ang II into the NTS. Both the slope and the intercept of the regression line function between delta HR and delta MAP were reduced by 43% from the control value of -1.55 +/- 0.13 beats/min/mm Hg (p less than 0.01) and -14 +/- 5 beats/min (p less than 0.05), respectively. Similar reductions were observed after Ang II administration into the fourth ventricle or intravenously, although microinjections into the cerebellum produced no effect. Endogenous blockade of Ang II by saralasin (22 ng) in the NTS facilitated the bradycardic response (-2.29 +/- 0.91 beats/min/mm Hg). Nitroprusside-induced tachycardia was not altered by Saralasin microinjection into the NTS or by Ang II application to the NTS, fourth ventricle, or intravenously.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Feb
PMID:Angiotensin II as a modulator of baroreceptor reflexes in the brainstem of conscious rats. 229 76

The impact of oral captopril, 2 mg . kg-1, on the dose and on the hemodynamic and hormonal effects of nitroprusside was studied in seven patients (Group II). A comparable group (Group I, n = 7) received nitroprusside alone. In both groups, nitroprusside produced comparable decreases in mean arterial pressure, systemic vascular resistance, and right atrial pressure; cardiac output increased because of a significant change in heart rate. Although plasma renin activity increased significantly (compared with control values) in both groups, it was greater (p = 0.01) through the operative period in patients pretreated with captopril. Plasma aldosterone concentration increased in Group I (p = 0.01) but decreased in Group II (p = 0.01). Plasma catecholamine concentrations increased (p = 0.01) with nitroprusside alone but were unchanged in captopril-treated patients. Plasma converting enzyme activity was markedly inhibited (p = 0.001) by captopril. Following cessation of nitroprusside infusion in Group I, rebound hypertension occurred in conjunction with a significant (p = 0.01) increase in systemic vascular resistance; it was associated with elevated plasma renin activity, catecholamines, and aldosterone concentrations. In contrast, captopril-treated patients showed no rebound hemodynamic changes. Nitroprusside dose was less (p = 0.01) with captopril pretreatment (2.1 +/- 0.3 vs. 4.8 +/- 0.9 microgram . kg-1 . min-1). Thus, captopril is a useful adjunct to nitroprusside-induced hypotension.
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PMID:Impact of captopril on hemodynamic and hormonal effects of nitroprusside. 241 94

Catecholamine and indoleamine metabolism in nucleus tractus solitarius were studied during drug-induced hypertension and hypotension. Urethane-anesthetized normotensive male Sprague-Dawley rats implanted with a 250-mu carbon paste in vivo electrochemical electrode were infused with phenylephrine to raise blood pressure 50 mm Hg. Other animals were given nitroprusside to lower pressure 20 mm Hg. Phenylephrine-induced hypertension was associated with a 30% reduction in the electrochemical peak corresponding to norepinephrine. The electrochemical peak which was identified as 5-hydroxyindoleacetic acid (5-HIAA) was increased 25% with the onset of hypertension and remain elevated after the phenylephrine infusion was stopped. Nitroprusside-induced hypotension resulted in a 20% reduction in the norepinephrine peak during the infusion followed by an additional 10% reduction after the infusion. 5-HIAA concentration did not change during the hypotensive phase but showed a 40% increase after the nitroprusside was stopped as blood pressure rebounded to levels higher than the control period. Direct tissue assays of norepinephrine and 5-HIAA confirmed the electrochemical findings. These experiments were repeated in rats which had undergone sinoaortic denervation. The electrochemical changes in norepinephrine and 5-HIAA associated with hypertension and hypotension were attenuated in these animals indicating that the brain neurotransmitter changes were a consequence of baroreceptor input to the brain. We conclude that 5-HIAA in nucleus tractus solitarius appears to be a marker for elevated blood pressure, whereas norepinephrine falls with either an increase or a decrease in pressure.
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PMID:Changes in arterial blood pressure lead to baroreceptor-mediated changes in norepinephrine and 5-hydroxyindoleacetic acid in rat nucleus tractus solitarius. 245 47

The effect of drug-induced hypertension and hypotension on neurotransmitter metabolism in the locus coeruleus (LC) of urethane anesthetized rats was studied using in vivo electrochemical methods. Peaks were seen at +0.15 V and +0.28 V. Studies with alpha-methylparatyrosine, fusaric acid and pargyline showed the first peak was produced by extracellular fluid dihydroxyphenylacetic acid (DOPAC) while the second peak was 5-hydroxyindoleacetic acid (5-HIAA). Phenylephrine was infused intravenously to raise the blood pressure by 50 mmHg, nitroprusside IV was used to reduce the blood pressure by 20 mmHg. During phenylephrine hypertension, the electrochemical signal for DOPAC showed an initial small reduction followed by a later significant increase which persisted even after the infusion was stopped. The signal for 5-HIAA rose with the onset of hypertension and remained elevated. Nitroprusside hypotension did not change the DOPAC peak but did lead to an immediate and persistent increase in the electrochemical 5-HIAA peak. To confirm the electrochemical findings, other groups of rats were decapitated during and after hypertensive and hypotensive drug infusions and the LC was assayed for norepinephrine, dopamine, DOPAC, serotonin, and 5-HIAA using HPLC with electrochemical detection. Changes in tissue DOPAC and 5-HIAA concentrations supported the electrochemical electrode observations. The effect of clonidine on the electrochemical recordings from LC was also studied. Clonidine reduced the catechol peak. No change was observed in the 5-HIAA peak during the infusion, but the 5-HIAA peak went up after the infusion was stopped. These experiments show that hypertension, hypotension, and alpha-2 agonists lead to changes in catecholamine and indoleamine metabolism in LC.
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PMID:Changes in neurotransmitter turnover in locus coeruleus produced by changes in arterial blood pressure. 246 Dec 45

Relationships between changes in levels of catechols and directly recorded sympathetic nerve activity were examined using simultaneous measurements of renal sympathetic nerve activity and arterial and renal venous concentrations of norepinephrine (NE), dihydroxyphenylalanine (dopa), and dihyroxyphenylglycol (DHPG) during reflexive alterations in renal sympathetic nerve activity in anesthetized, adrenal-demedullated rats. Nitroprusside infusion increased renal sympathetic nerve activity by 90%, arterial levels of dopa by 96%, NE by 326%, and DHPG by 141%. Phenylephrine infusion increased arterial DHPG levels by 81% and decreased renal sympathetic nerve activity by 37% and NE levels by 26%; arterial dopa levels were unchanged. Ganglionic blockade by chlorisondamine (with concomitant phenylephrine infusion to maintain MAP) decreased renal sympathetic nerve activity by 65% and NE concentrations by 37%; arterial dopa concentrations were unchanged, and DHPG concentrations increased by 60%. Proportionate responses of arterial levels of NE were strongly related to proportionate changes in renal sympathetic nerve activity. Clearance of DHPG from arterial plasma was prolonged by phenylephrine-induced hypertension and by nitroprusside-induced hypotension. The results suggest that changes in arterial NE levels reflect changes in sympathetic activity; changes in dopa levels reflect changes in catecholamine biosynthesis; and changes in DHPG levels depend on reuptake of released NE and on hemodynamic factors affecting DHPG clearance.
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PMID:Plasma levels of catechols during reflexive changes in sympathetic nerve activity. 250 66

In a randomized study, labetalol-induced hypotension and nitroprusside-induced hypotension were compared in 20 patients (10 in each group) scheduled for major orthopedic procedures. Each patient was subjected to an identical anesthetic protocol and similar drug-induced reductions in mean arterial blood pressure (BP) (50 to 55 mmHg). Nitroprusside infusion was associated with a significant (p less than 0.05) increase in heart rate and cardiac output; rebound hypertension was observed in three patients after discontinuation of nitroprusside. Labetalol administration was not associated with any of these findings. Arterial PO2 decreased in both groups. It was concluded that labetalol offers advantages over nitroprusside.
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PMID:A randomized comparison of labetalol and nitroprusside for induced hypotension. 269 5

Twenty-five patients scheduled for lumbar fusion or cerebrovascular surgery were enrolled in an open label treatment controlled study comparing blood pressure and heart rate responses during deliberate hypotension with either esmolol or nitroprusside during steady-state N2O/isoflurane anesthesia. The first 5 patients were empirically assigned to the esmolol group; the remaining 20 patients were randomized to receive either esmolol or nitroprusside. The target of 15% reduction in mean arterial pressure (MAP) from baseline determined during anesthesia was attained with esmolol 195 +/- 10 micrograms/kg/min (mean +/- SEM) for the group (n = 15) or nitroprusside 1.9 +/- 0.3 micrograms/kg/min for the nitroprusside group (n = 10). Nitroprusside use was associated with a 15.9 +/- 5.3% increase in heart rate compared to a 12.1 +/- 2.2% decrease in the esmolol group (p = 0.0001 between groups). Upon termination of the hypotensive infusions, nitroprusside patients had a MAP increase of 13.9 +/- 5.5% above baseline (p less than 0.05 compared to prehypotension) while the 7.4 +/- 3.5% increase in the esmolol group was not statistically significant. Although 30% of nitroprusside patients overshot their baseline MAP by more than 25%, no esmolol patients had this degree of rebound. One esmolol patient had a brief period of atrial premature contractions. No patient in either group suffered any adverse reaction to hypotension. It is concluded that in moderate doses esmolol is a safe and effective hypotensive agent during isoflurane anesthesia, with no reflex tachycardia and no significant potential for rebound hypertension. A MAP reduction of 30% from preanesthesia baseline was readily obtained with this combination.
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PMID:A controlled trial of esmolol for the induction of deliberate hypotension. 290 83

The release of vasopressin, renin, and catecholamines by the fetus during either maternal or fetal hypotension was examined in chronically catheterized fetal lambs. Nitroprusside was infused intravenously for 1 h into seven pregnant ewes (maternal hypotension) or nine fetal lambs (fetal hypotension); the rates were adjusted to achieve a 15 to 30% decrease in mean blood pressure. During maternal hypotension, mean +/- SE vasopressin in maternal plasma increased from 1.2 +/- 0.2 pg.ml-1 to 208 +/- 153 pg.ml-1 and plasma renin activity increased from 1.5 +/- 0.3 ng.ml-1.h-1 to 6.6 +/- 1.6 ng.ml-1.h-1. Fetal vasopressin and plasma renin activity also increased during the same interval from 1.1 +/- 0.3 to 16.9 +/- 7.5 pg.ml-1 and 3.7 +/- 1.1 to 10.5 +/- 2.85 ng.ml-1.h-1, respectively; but no changes were observed in fetal blood pressure, heart rate, or acid base status. During fetal hypotension, mean vasopressin in fetal plasma increased from 4.3 +/- 3.4 pg.ml-1 to 1054 +/- 772 pg.ml-1, plasma renin activity increased from 5.7 +/- 2.2 ng.ml-1 to 22.2 +/- 7.1 ng.ml-1.h-1, and total catecholamines from 174 +/- 58 pg.ml-1 to 810 +/- 416 pg.ml-1. There was no change in fetal heart rate, acid base status, osmolality, or sodium concentration. The fetus became and remained hypertensive for at least 1 h after the end of infusion. This prolonged hypertension was associated with elevated levels of vasopressin and plasma renin activity. Peak vasopressin levels were proportional to the total nitroprusside dose in both the ewe and fetus (maternal r = 0.796, fetus r = 0.870).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma vasopressin, renin, and catecholamines during nitroprusside-induced maternal and fetal hypotension in sheep. 304 42

The relationship between early hypertension following carotid endarterectomy, and intraoperative cerebral ischemia was investigated. Two measures of the adequacy of collateral cerebral circulation during carotid clamping were used: collateral cerebral perfusion pressure (delta P), and the ratio of collateral to ipsilateral cerebral vascular resistance (R/R). Change in blood pressure was measured by the ratio of mean early post to preendarterectomy pressure (P/P). Nitroprusside or nitroglycerin (NN) was used after endarterectomy to maintain systolic blood pressure less than 160 mmHg. The mean values for NN (n = 26) and no NN (n = 81) groups were: delta P = 30.0 and 40.2 mmHg (p less than 0.001); R/R = 1.93 and 1.24 (p less than 0.005); and P/P = 1.03 and 0.857 (p less than 0.001 p by unpaired t test). Linear regression analysis of the two measures of cerebral perfusion with the ratio of post-to preoperative blood pressure gave correlation coefficients between 0.629 and 0.841 with a probability that the slope of the regression line greater than 0 of less than 0.01. Low delta P and high R/R correlate with early postcarotid endarterectomy hypertension. These results support the hypothesis that one determinant of early post endarterectomy hypertension is inadequate collateral cerebral circulation during carotid clamping.
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PMID:The relationship of early hypertension following carotid endarterectomy to intraoperative cerebral ischemia. 314 94

We report the case of a 46-year-old woman who took approximately 8 mg of clonidine in a suicidal gesture. She arrived in the emergency department 45 min after the overdose with severe hypertension and an altered mental status. Nitroprusside, which is the drug of choice for treating this "paradoxical hypertension," was not readily available. The patient was treated with a total of 20 mg of nifedipine sublingually. This resulted in a rapid decline in her blood pressure and an improvement in her mental status. We review the toxicology of clonidine overdose and discuss its treatment.
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PMID:The use of sublingual nifedipine in a patient with a clonidine overdose. 329 Mar 24


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