Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The forearm blood flow (FABF) and other cardiovascular responses of 20 black men with a parental history of hypertension were compared with the responses of 18 black men without a parental history of hypertension. The results showed that sons of hypertensive parents had higher systolic (SBP) and diastolic (DBP) blood pressure than sons of normotensive parents during the initial assessment as well as significantly higher self-determined home SBP. Sons of hypertensive parents had higher SBP responses than sons of normotensive parents during mental challenge and the cold pressor, but there were no group differences in DBP, heart rate (HR), (FABF), or forearm vascular resistance (FAVR) responses to the stressors. Significant positive correlations between HR and FABF responses to the stressors were observed for sons of hypertensive parents. Finally, the results showed that the BP and FAVR responses to the cold pressor (a painful task that elicits alpha-adrenergic activity) were significantly higher than responses to mental challenge (a task that elicits beta-adrenergic activity) for both groups. The implications of these results are discussed in light of current research suggesting that blacks may have a greater tendency toward BP responses mediated by alpha-adrenergic increases in vascular resistance.
 ...
PMID:Cardiovascular reactivity to stress in black male offspring of hypertensive parents. 192 54

The effects of antiarrhythmic doses of lidocaine on efferent sympathetic outflow or sympathetic responses to autonomic stimuli in humans are unknown. In the present study, direct recordings of postganglionic muscle sympathetic nerve activity (MSNA), which modulates vascular tone, were obtained from the peroneal nerve of 22 healthy volunteers (aged 20 to 27 years). Baseline cardiac intervals (ECG), arterial pressure (radial artery), central venous pressure (CVP, jugular vein), forearm vascular resistance (FVR, Hg-in-Silastic plethysmography), and MSNA were identical in two randomized study groups (lidocaine [L], 1.5 mg/kg bolus, followed by 2 mg/min infusion, n = 12; and placebo [P] saline bolus and infusion, n = 10). Each underwent a cold pressor test (CPT, ice packs to foot for 90 seconds) and baroreceptor test (sequential boluses of 100 micrograms of sodium nitroprusside and 100 micrograms of phenylephrine). Five minutes after the bolus administration of L, plasma L levels were 3 micrograms/mL, which was associated with significant (P less than 0.05) increases in systolic and diastolic pressures (6.6 +/- 2.4 and 5.5 +/- 1.1 mm Hg). This elicited significant reflex decreases in MSNA (-3 +/- 1.1 bursts/100 cardiac cycles) and RR interval (-63 +/- 14 ms). The hypertension, tachycardia, forearm vasoconstriction, and MSNA increase in response to the CPT were significantly attenuated and the sympathoexcitatory response to baroreceptor unloading was blunted by L. These responses were not altered during the administration of P. In the steady-state L infusion period, plasma levels were subtherapeutic (1 microgram/mL) and were insufficient to consistently alter autonomic stress responses.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Lidocaine attenuates efferent sympathetic responses to stress in humans. 193 48

This article presents some aspects of the role of sympathetic efferent nerves in the regulation of blood pressure in humans. Lessons have been learned from disorders that cause either sympathetic underactivity or overactivity. In chronic autonomic failure, pressor stimuli (mental arithmetic, isometric exercise, or cold) are unable to raise blood pressure, whereas stimuli that normally activate sympathetic efferent nerves to maintain blood pressure (head-up tilt, exercise, and food ingestion) can cause marked hypotension. Recognition of specific defects, such as the inability to synthesize norepinephrine in isolated dopamine beta-hydroxylase deficiency, suggests that sympathetic nerves may influence blood pressure regulation through nonadrenergic mechanisms (dopamine, neuropeptides, and purines). Tetraplegic patients with high cervical cord transection also have sympathetic impairment and postural hypotension, but this is less of a clinical problem because of compensatory hormonal and other mechanisms. Tetraplegic patients are unique as they also may have severe paroxysmal hypertension because of increased spinal sympathetic reflex activity. The pathophysiological mechanisms responsible for this exaggerated response include changes in postsynaptic adrenergic receptor numbers and their sensitivity, the actions of nonadrenergic cotransmitters, and the lack of sympathoneural pathways from the brain that are severed by the lesion. Finally, the putative role of the sympathetic nervous system in hypertension with unilateral renal artery stenosis, which initially is humorally mediated, is discussed. The centrally acting sympatholytic agent clonidine is effective in lowering blood pressure in renovascular hypertension independently of humoral factors when multiple agents have failed.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Nov
PMID:Role of sympathetic efferent nerves in blood pressure regulation and in hypertension. 193 84

In anesthetized and artificially ventilated rats, passive or reflex hypertension was produced by ligation of the abdominal aorta (12 rats), or sudden lowering of the cutaneous temperature to 25-30 degrees C achieved by exposure to cold water (26 rats), respectively. Cold exposure increased the blood flow (microsphere method) in all of the brain regions studied by 54-174% in the face of a reflex increment in the arterial pressure by 40% on average. The vascular resistance was changed by 0-(-)32%. Such hemodynamic alterations were greater in almost all of the brain regions than would be anticipated from the autoregulatory function of the brain circulation, as evidenced by a comparison with those observed during passive hypertension. Exposure to thermoneutral water resulted in the minimal changes in the hemodynamic states of the systemic as well as brain circulations (5 rats). The sympathetic nerves innervating the cranial vessels were strongly activated during the cold exposure, as confirmed by the observation of a large increase in flow in the temporalis muscle after acute surgical sympathectomy. However, sympathetic denervation did not alter the degree of hemodynamic changes occurring in the brain regions during cold exposure. We conclude that, in the face of reflex hypertension induced by cold exposure, the powerfully activated sympathetic nerves failed to exert their well-known effect on the brain blood flow which prevents it from rising to an excessively high level.
 ...
PMID:Hyperperfusion of the rat brain during reflex hypertension induced by sudden lowering of the cutaneous temperature. 194 31

This study was designed to assess the effect of chronic dietary administration (2.5 and 5.0% by weight) of the neutral amino acid, L-tryptophan, on the development of hypertension during chronic exposure to cold. In addition, a warm-adapted and cold-treated control group receiving unsupplemented food were used. Chronic administration of the lower dose of L-tryptophan (850 mg/day) prevented the elevation of blood pressure attenuated cardiac hypertrophy, and had no effect on body weight during exposure to cold. The higher dose of L-tryptophan (1,690 mg/day) attenuated the rate of blood pressure increase, did not affect cardiac hypertrophy, attenuated the gain in body weight, and increased the urinary output of epinephrine. Thus, this dose may be associated with some toxicity. Both doses of tryptophan failed to prevent certain other responses characteristically occurring during exposure to cold: i.e. increased weight of the kidneys, adrenal glands and brown adipose tissue; increased food and water consumption; increased dipsogenic responsiveness to angiotensin II, and increased plasma aldosterone concentration. The results indicate that chronic dietary administration of L-tryptophan (850 mg/day) can prevent the development of cold-induced hypertension, as it can in all other models of hypertension tested thus far in rats.
 ...
PMID:Effect of chronic dietary treatment with L-tryptophan on the development of cold-induced hypertension in rats. 194 99

Previous studies have shown that urinary N-acetyl-beta-glucosaminidase (NAG) is elevated in patients with hypertension, even without renal disease. To elucidate the value of measuring NAG, both in urine and serum of hypertensive patients, we measured NAG activity in the serum, plasma, and 24-hour urine by the fluorimetric method in 84 patients with uncomplicated essential hypertension before and after 6 months of effective treatment. NAG activities of these hypertensive patients were compared with those of 102 healthy normotensive subjects and 97 patients with various renal diseases and controlled hypertension. Serum NAG activity was clearly greater in patients with essential hypertension (427 +/- 124 U/mL) than in normotensive subjects (380 +/- 109 U/mL) or patients with renal disorders (393 +/- 115 U/mL) (P less than or equal to 0.004). The greater was the diastolic pressure in the hypertensive group, the greater was serum NAG activity (r = +0.30, P = 0.004). Hypertensive patients with high serum NAG activity were further characterized by a more exaggerated increase in systolic pressure (34 +/- 16 v 25 +/- 15 mm Hg, P = 0.051) and total peripheral resistance (19% +/- 18% v 12% +/- 13%, P = 0.042) in response to the cold pressor test and by a greater increase in systolic pressure (56 +/- 15 v 45 +/- 13 mm Hg, P = 0.009) and diastolic pressure (11 +/- 7 v 6 +/- 9, P = 0.043) in response to bicycle exercise testing than the group with low serum NAG activity. In contrast, urinary NAG activity tended to be only slightly higher in patients with essential hypertension than in the normotensive control group (33 +/- 31 v 23 +/- 29 U/mg creatinine [cr], P = 0.062), whereas patients with renal diseases had clearly increased urinary NAG activity (87 +/- 105 U/mg cr) (P less than 0.001). Following effective antihypertensive therapy, serum NAG activity decreased in patients with essential hypertension to values of normotensive control subjects (from 427 +/- 124 U/mL to 386 +/- 106 U/mL, P less than 0.01). A significant decrease in serum NAG activity was observed in patients with both initially high as well as low pretreatment serum NAG activities (P less than 0.001 and P less than 0.02, respectively). Urinary NAG activity overall was unchanged by antihypertensive treatment. We conclude that in patients with mild essential hypertension, serum NAG activity was already elevated (whereas urinary NAG activity was not) and was normalized by effective antihypertensive treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Elevated serum activity of N-acetyl-beta-glucosaminidase in essential hypertension: diagnostic value and reversal to normal values after antihypertensive therapy. 196 47

Previous biochemical assessment of sympathetic nervous system activity including plasma catecholamines, plasma renin activity, and plasma dopamine-beta-hydroxylase levels has suggested racial differences in the contribution of the sympathetic nervous system to the pathogenesis or maintenance of hypertension. We, therefore, performed physiological and pharmacological studies in white and black subjects with essential hypertension and their age-matched normotensive counterparts to assess autonomic and sympathetic nervous system function. One hundred one male subjects (47 white hypertensive, 17 black hypertensive, 22 white normotensive, and 15 black normotensive subjects) were evaluated for baroreceptor reflex sensitivity to low-pressure (amyl nitrite inhalation) and high-pressure (phenylephrine infusion) stimuli; cold pressor test heart rate and blood pressure responses; and blood pressure response to phentolamine alpha-adrenergic blockade. Hypertensive subjects exhibited an increase in resting heart rate, a decrease in baroreceptor reflex sensitivity, and an exaggerated decline in mean arterial pressure in response to phentolamine. These abnormalities were present to a comparable degree in black and white hypertensive subjects. Cold pressor testing revealed greater increases in heart rate in blacks as compared with whites; however, this racial difference was present regardless of blood pressure status, occurring in black normotensive and black hypertensive subjects to a comparable degree. Cold pressor test blood pressure increments were similar in the four groups. We conclude that both white hypertensive and black hypertensive subjects demonstrate similar abnormalities in autonomic and sympathetic nervous system function including blunting of baroreceptor reflex sensitivity and an increased alpha-adrenergic receptor participation in blood pressure maintenance. The results do not suggest major racial differences in autonomic pathogenetic mechanisms in hypertension.
 ...
PMID:Autonomic function in hypertension. Are there racial differences? 196 34

Overweight and obesity may develop in individuals with genetically determined low resting energy expenditure. Drugs are among the recognised precipitating factors. The obesity promoting impact of beta-blockers is, however, less well known. Resting energy expenditure, and thermogenesis induced by stimuli such as meals, cold and heat exposure, stress and anxiety, have a facultative component mediated by the sympathoadrenal system through catecholamines working on beta-adrenoceptors. Treatment with beta-blockers reduces the facultative thermogenesis by 50-100 kcal/d, which corresponds to the weight gain of 2-5 kg/year reported in clinical trials. Treatment with beta-blockers also results in insulin resistance, which may aggravate existing diabetes and elicit diabetes in predisposed patients. Overweight and obesity are frequently complicated with hypertension and angina pectoris, which are often treated with beta-blockers. Obesity is associated with a defective sympathetic activity, and treatment with beta-blockers may further reduce facultative thermogenesis and promote weight gain. The consequence may be aggravation of hypertension, insulin resistance and other atherogenic factors. The causal therapy of android overweight and obesity complicated with diabetes or hypertension is a sufficient weight loss. If pharmacological treatment is inevitable, combined treatment with diuretics and ACE-inhibitors are most appropriate.
 ...
PMID:[Obesity and diabetes as side-effects of beta-blockers]. 197 28

Beta-adrenoceptor antagonists (beta blockers) are a well-established first-line treatment for hypertension, but they have been associated with unwanted symptoms including cold extremities, lethargy, and nightmares. Ketanserin is a serotonin S2-receptor antagonist that has previously been shown to reduce blood pressure in hypertensive patients by reducing systemic vascular resistance. Hypertensive patients whose sitting diastolic blood pressure was greater than or equal to 95 mmHg, despite at least 4 weeks therapy with an optimal dose of beta blocker, were selected for the study. The beta-blocker dose remained constant throughout the study, but patients were randomly allocated to receive ketanserin 20 mg twice daily, ketanserin 40 mg twice daily, or bendrofluazide 5 mg each morning plus placebo at night in addition to the beta-blocker therapy. One hundred and forty two patients completed the symptom questionnaire at randomization and after 12 weeks treatment. The treatment groups were well matched for age, sex, weight, and blood pressure. Blood pressure was reduced significantly by all treatments, and there were no between-group differences. Bendrofluazide adversely affected alertness (p less than 0.05) and concentration (p less than 0.01) whereas ketanserin had no significant effect and the ketanserin 20 mg twice daily group had better concentration than the bendrofluazide group (p less than 0.05). Ketanserin treatment reduced the incidence of nightmares (p less than 0.05 for 20 mg twice daily and 40 mg twice daily) and was an improvement over bendrofluazide treatment in this respect (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Serotonin antagonism reduces the adverse symptoms of beta blockade. 198 Oct 22

Retrospective experience with drug therapy in 747 patients with essential hypertension registered from 1972-1983 is reported. Five hundred patients were seen between 1972 to 1978 and 247 between 1979-1983; the latter group was characterised by the use of beta blockers as first line drugs. Hypertension was graded according to level of diastolic blood pressure as mild, moderate and moderately severe or severe in 423, 211, and 113 patients, respectively. The overall response to treatment at 6 months was satisfactory in 66.2% of mild, 50.2% of moderate and 58.4% of severe grades of hypertension. A large number of patients in both the groups having varying grades of severity needed at least 2 to 3 drugs for the control of hypertension. The side effects of drugs were generally mild which included general weakness with diuretics; skin rash, nasal congestion and pruritus with methyldopa; cold extremities with beta blockers and palpitations with prazosin.
 ...
PMID:Experience with anti-hypertensive drug therapy in a hypertension clinic--1972-1983. A retrospective analysis. 198 Oct 83


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>