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

The short-term effects of pressor amines were investigated in four patients with postural hypotension caused by autonomic failure. In supine patients p-tyramine alone or with a monoamine-oxidase inhibitor produced pronounced supine hypertension without abolishing the symptoms associated with a postural fall in blood-pressure. Phenylephrine or ephedrine maintained a normal blood-pressure on standing but caused supine hypertension. Thus the effects of p-tyramine with or without a monoamine-oxidase inhibitor were unpredictable and did not include relief of postural hypotension. Phenylephrine or ephedrine had some beneficial effect, but since all these drugs influence standing pressure only at the expense of pronounced supine hypertension, alternative therapy must be sought.
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PMID:Pressor amines and monoamine-oxidase inhibitors for treatment of postural hypotension in autonomic failure. Limitations and hazards. 7 3

Human hypertension has been related to abnormalities of autonomic blood pressure regulation. In order to characterize a possible defect, we have studied several aspects of reflex autonomic circulatory control in normal subjects, patients with primary hypertension, and two types of subjects with uremia and elevated blood pressure. Phenylephrine infusion (a measurement of baroreceptor response to high pressure stimulus) resulted in similar hemodynamic changes in all types of subjects. However, all groups of patients exhibited significantly different hemodynamic responses to amyl nitrite inhalation (an index of baroreceptor response to low pressure stimulus). These results suggest that patients with uremia and those with primary hypertension differ from each other and normal subjects regarding baroreceptor reflex function. Furthermore, one type of uremic patient may have a neurogenic component to their hypertension similar to experimental animals following surgical section of afferent baroreceptor nerves.
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PMID:Baroreflex function in uremic and hypertensive man. 72 17

Our previous studies have suggested that atrial natriuretic peptide in the caudal nucleus tractus solitarii is involved in the centrally mediated regulation of blood pressure in the salt-sensitive spontaneously hypertensive rat (SHR). The current study tested the hypothesis that endogenous atrial natriuretic peptide in the caudal nucleus tractus solitarii participates in baroreceptor reflex control of heart rate in this hypertensive model. Salt-sensitive SHR and control Wistar-Kyoto (WKY) rats maintained on basal (1%) salt intake were studied. Arterial baroreceptor reflex-mediated changes in heart rate were recorded in conscious unrestrained rats during phenylephrine (5-40 micrograms.kg-1.min-1 infusion; 30 minutes later, atrial natriuretic peptide (50 ng), monoclonal antibody to atrial natriuretic peptide (0.55 micrograms), purified mouse immunoglobulin G (0.55 micrograms), or artificial cerebrospinal fluid vehicle (50 nl) was microinjected into the caudal nucleus tractus solitarii. Phenylephrine infusion was then repeated and mean arterial pressure and heart rate were monitored as before. The slope of the heart rate/mean arterial pressure relation was significantly less (p less than 0.05) in the salt-sensitive SHR than in the WKY control, indicating that baroreceptor reflex control of heart rate was blunted in this hypertensive model. Microinjection of atrial natriuretic peptide into the caudal nucleus tractus solitarii further blunted (p less than 0.05) baroreceptor reflex control of heart rate in salt-sensitive SHR but not in WKY rats. In contrast, microinjection of the monoclonal antibody enhanced the sensitivity of baroreceptor reflex control of heart rate in salt-sensitive SHR but not in WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Sep
PMID:Atrial natriuretic peptide modulates baroreceptor reflex in spontaneously hypertensive rat. 138 31

To determine alpha 1-adrenergic receptor responsiveness of the renal vasculature in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR), phenylephrine (2.5 or 5.0 micrograms.kg-1.min-1 iv) or saline was infused. Effective renal blood flow (ERBF) and glomerular filtration rate were determined by p-aminohippuric acid and inulin clearances, respectively. Peritubular capillary, proximal tubular, and stop-flow pressures (SFP) were measured by micropuncture. Phenylephrine decreased ERBF (6.27 +/- 0.48 to 4.55 +/- 0.65 ml.min-1.g-1; P less than 0.05) and increased arterial pressure and SFP (31.5 +/- 0.9 to 34.2 +/- 1.0 mmHg) in SHR. It only increased arterial pressure and ERBF in WKY without changing SFP. Afferent arteriolar resistance (RA) and glomerular capillary pressure (PG) remained unchanged, whereas efferent resistance (RE) decreased in WKY; in contrast, RA, RE, and PG increased in SHR (RA 21.2 +/- 2.0 to 38.1 +/- 7.1 mmHg.ml-1.min.g, RE 6.9 +/- 0.6 to 13.9 +/- 3.8 mmHg.ml-1.min.g; and PG 49.6 +/- 0.9 to 53.7 +/- 1.1 mmHg; all P less than 0.05). These data demonstrated increased SHR afferent and efferent arteriolar responsiveness; WKY efferent arteriolar hyperresponsiveness was not observed. The findings support the concept of augmented intrarenal vascular alpha 1-adrenergic responsiveness in hypertension that may predispose to subsequent glomerular hypertension.
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PMID:Spontaneously hypertensive rats demonstrate increased renal vascular alpha 1-adrenergic receptor responsiveness. 185 27

Muscle sympathetic nerve activity (MSNA) in humans is regulated in part by arterial baroreceptors. However, although mental stress increases blood pressure, it also increases MSNA. This suggests that baroreceptor control of MSNA is altered during mental stress. In nine healthy men (age range, 20-26 years), we recorded heart rate, blood pressure, and efferent MSNA (peroneal nerve, microneurography) during a 4-minute mental arithmetic task performed both before and during infusion of phenylephrine sufficient to markedly suppress resting MSNA. Before phenylephrine, mental stress significantly increased mean blood pressure (p less than 0.01), heart rate (p less than 0.01), and MSNA (from 18.5 +/- 3.2 to 24.8 +/- 3.5 bursts/min, p less than 0.001). Phenylephrine infusion increased resting mean blood pressure (from 84.0 +/- 2.6 to 90.0 +/- 2.7 mm Hg, p less than 0.01) and decreased resting heart rate (from 65.6 +/- 1.7 to 55.6 +/- 2.0 beats/min, p less than 0.01). Resting MSNA decreased dramatically during phenylephrine (from 18.5 +/- 3.2 to 3.3 +/- 1.3 bursts/min, p less than 0.01). During phenylephrine, mental stress again significantly (p less than 0.01) increased mean blood pressure, heart rate, and MSNA (from 3.1 +/- 1.4 to 10.9 +/- 1.8 bursts/min). The magnitude of stress-induced increases in MSNA and heart rate were comparable before and during phenylephrine infusion despite the greater elevation in diastolic pressure during stress plus phenylephrine. The present study demonstrates that mental stress produces sympathoexcitatory and pressor responses even during sustained stimulation of arterial baroreceptors.
Hypertension 1991 Apr
PMID:Mental stress increases sympathetic nerve activity during sustained baroreceptor stimulation in humans. 201 92

An increased urinary excretion of thromboxane (Tx)B2 (Geoffroy & al., Hypertension 1986, 4 suppl 3: S37) and an elevated renal sympathetic activity (Sautel & al., Am J Physiol 1988, 255: H736) were simultaneously observed in the developing genetically hypertensive rat of the Lyon strain (LH). In the present work, the relationship between the adrenergic stimulation and prostaglandins (PGs) release was studied using isolated perfused kidney of 8 week-old LH rats and their normotensive controls (LN). Phenylephrine (PHE, 5 - 190 x 10(-8) M) and norepinephrine (NE, 1.2 - 96 x 10(-8) M) were administered in a single pass kidney perfused with a cell free solution and their effects were studied on the renal vascular resistances (RVR) and urinary excretion of TxB2 and 6-keto-PGF1 alpha (6KPGF) measured by specific radioimmunoassays after separation by HPLC. The results (mean +/- SE) obtained before (C) and after PHE and NE perfusions at concentrations: D1 = 31 and 10.5; D2 = 190 and 96 10(-8) M for PHE and NE respectively (* p less than 0.05 ** p less than 0.01 *** p less than 0.001 LH vs LN) were as follows: [table: see text] During the control period, kidneys of LH rats exhibited increased RVR when compared to LN controls but a similar PG excretion. The 2 concentrations of PHE and NE used which produced a similar increase in RVR strikingly stimulated the PG excretion. This effect which was more marked for NE than for PHE did not differ between the 2 strains for 6KPGF but was enhanced for TxB2 in kidney of LH rat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adrenergic stimulation and renal synthesis of prostaglandins in genetically hypertensive rats of the Lyons strain]. 212 61

Hypertensive patients have reduced lymphocyte beta-adrenergic responsiveness which is corrected by a low sodium (Na) diet. To determine if this represents a more generalized abnormality in beta adrenoceptor response, we studied beta adrenergic-mediated vasodilation in hand veins of borderline hypertensive subjects and controls. Subjects received a 5-d diet containing high Na/low potassium (K), high Na/high K, or low Na/high K. Venous distension, as evaluated by a linear variable differential transformer, was measured in relation to infusion of phenylephrine followed by isoproterenol and nitroglycerin. On both the high Na/high K and high Na/low K diets, hypertensive subjects had significantly decreased isoproterenol-mediated vasodilation (47% decrease, P less than 0.01 and 36% decrease, P less than 0.01, respectively). On the low Na/high K diet, isoproterenol-mediated vasodilation in hypertensive subjects increased 41% (P less than 0.01) to a level not different from controls. Nitroglycerin-mediated vasodilation was not different in normotensive and hypertensive subjects, nor was it altered with Na intake. Phenylephrine-mediated vasoconstriction did not differ between normotensive and hypertensive groups. Venous beta-adrenergic response correlated with lymphocyte beta adrenoceptor density in normotensive (r = 0.53, P less than 0.005) but not hypertensive subjects. This study demonstrates that beta-adrenergic responsiveness is selectively reduced in peripheral veins of borderline hypertensive subjects, and this is corrected by a low Na diet. In view of our previous findings of reduced lymphocyte beta-adrenergic responsiveness in borderline hypertension, these studies suggest a generalized defect of beta adrenoceptor responsiveness in human hypertension. Further, dietary Na may play an important role in regulating this abnormality.
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PMID:Defective venous beta-adrenergic response in borderline hypertensive subjects is corrected by a low sodium diet. 215 21

The effects of the calcium antagonist nisoldipine on contractions stimulated by phenylephrine and B-HT 920 (agonists of alpha 1- and alpha 2-adrenoceptors) in isolated aortic rings from stroke-prone spontaneously hypertensive rats (SHRSP) and from normotensive Wistar-Kyoto rats (WKY) were investigated in vitro. Phenylephrine and B-HT 920 produced concentration-dependent contractions of vessels from both groups of animals. The absolute force of the contractions was less in the aortae from hypertensive rats after all doses of both agonists. Nisoldipine inhibited the B-HT 920-induced contraction much more in vessels from SHRSP than in those from normotensive WKY rats (IC50 = 1.5 X 10(-10) versus 7 X 10(-9) g/ml). The phenylephrine contractions were inhibited in SHRSP aortae by higher concentrations (IC50 = 8.5 X 10(-8) g/ml) of nisoldipine; in WKY, nisoldipine only produced a slight inhibition of phenylephrine-induced contractions. The inhibitory concentrations of nisoldipine on BHT-920-induced contractions are similar to those for the inhibition of the calcium or depolarization-induced contractions in other experiments. The alpha 2-agonist-induced contractions of rat aorta are dependent on transmembrane calcium supply. The higher efficacy of nisoldipine in aortae from SHRSP suggests an increased transmembrane availability of calcium ions in hypertension.
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PMID:Interference of the calcium antagonist nisoldipine with the abnormal response of vessels from hypertensive rats to alpha-adrenergic stimulation. 241 97

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


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