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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 hypertension on DNA content of isolated aortic smooth muscle cells and their nuclei has been studied in Wistar rats treated with deoxycorticosterone and salt (DOC/salt). Eight weeks of DOC/salt administration induced a significant increase in aortic smooth muscle cells with tetraploid nuclei from 9.7 +/- 0.8% (mean +/- SE) in control animals to 26.6 +/- 2.4% with DOC/salt. The tetraploid cells appeared approximately 60% larger in size than diploid cells as estimated by forward light scatter. Prolonged reversal of hypertension by withdrawal of DOC/salt for 3 months did not reduce nuclear tetraploidy significantly but appeared to prevent further increases. The results suggest that hypertension influences the growth cycle of aortic smooth muscle cells and increases nuclear polyploidy and cellular hypertrophy. Preliminary studies have also been performed to measure transmembrane potential in isolated viable aortic smooth muscle cells with a lipophilic cationic fluoroprobe, 3,3 dipentyloxacarbocyanine, which distributes into cells in a potential-dependent manner. Norepinephrine (10(-6)M to 10(-3)M) appeared to produce a concentration-dependent reduction in membrane potential that was blocked by equimolar concentrations of prazosin but not of yohimbine. The studies suggest that norepinephrine can cause depolarization of smooth muscle cells through an alpha 1-mediated mechanism.
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PMID:Effects of deoxycorticosterone/salt hypertension on cell ploidy in rat aortic smooth muscle cells. 379 14

The pressor interactions between angiotensin II and norepinephrine were investigated in conscious New Zealand white rabbits receiving a low sodium diet. Angiotensin II was administered continuously by intraperitoneal osmotic pumps in a subpressor dose so as to avoid the potentially confounding effects of experimentally-induced hypertension. Norepinephrine challenges were given as a series of graded intravenous boluses. During the 3 days of study the baseline blood pressure in the angiotensin-treated rabbits (n=10) did not differ from that in controls (n=10) whose intraperitoneal pumps contained only diluent. After 24 hours the systolic and diastolic blood pressure responses to norepinephrine in the angiotensin-treated group were, on average, 45% and 30% higher than in the controls; after 72 hours, they were 46% and 34% higher. Although the pressor amplitudes were increased by angiotensin II, they were not prolonged. Thus, facilitation by the subpressor angiotensin II of the blood pressure responses to norepinephrine did not seem dependent upon alterations in endogenous sympathetic mechanisms or the uptake of norepinephrine; nor could it be explained by sodium retention. It is possible that angiotensin II exhibits its effect by enhancing contractile responsiveness to norepinephrine at the postreceptor level.
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PMID:Enhancement of the pressor response to norepinephrine by angiotensin in the conscious rabbit. 388 83

The effect of desoxycorticosterone (DOC)-NaCl treatment upon sympathetic neuronal uptake of norepinephrine (uptake1) was evaluated in strains of hypertension-resistant (SBN) and -prone (SBH) rats. Uninephrectomized animals were given either a placebo pellet sc and tapwater (untreated) or a 25-mg DOC pellet and 1% NaCl. Four weeks later, tail systolic pressure was significantly higher in DOC-NaCl SBH, 183 +/- 3 mm Hg, than SBN, 141 +/- 2 (P less than 0.01). [3H]Norepinephrine (NE) uptake was determined in heart slices of all four groups by incubation in Krebs buffer at 37 degrees C for 20 min at several concentrations. Preliminary studies confirmed that this is a measure of uptake1. Heart slices of DOC-NaCl-treated SBN and SBH rats had significantly reduced NE uptake at concentrations of 10-80 nM (P less than 0.01); there was no significant difference between SBN and SBH in this regard. Untreated SBH rats have been shown to have a defect in baroreflex regulation when normotensive. The results raise the possibility that the greater increase in arterial pressure caused by DOC-NaCl in SBH compared to SBN may be related to both the inborn difference in reflex function and an acquired reduction in inactivation of norepinephrine by sympathetic neuronal uptake.
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PMID:Reduced sympathetic neuronal uptake (uptake1) in a genetic model of desoxycorticosterone-NaCl hypertension. 396 82

To determine whether altered vascular reactivity could contribute to hypertension after repair of coarctation, the change in forearm and calf vascular resistances to small intra-arterial infusions of norepinephrine were measured in six patients who had undergone surgical correction of coarctation of the aorta but still had upper extremity hypertension and compared with similar measurements made in five normotensive patients with mild heart disease. Only the mean upper extremity pressure was significantly greater in the group that underwent repair of coarctation (102 +/- 11 vs 83 +/- 5 mm Hg, p less than .05, for mean arm pressures and 96 +/- 13 vs 83 +/- 7 mm Hg for mean leg pressures in patients who had coarctation vs normotensive patients, respectively). Forearm and calf blood flows were measured in the right arm and leg with a mercury-in-plastic strain-gauge plethysmograph. Forearm and calf vascular resistances were calculated by dividing mean arterial pressure of the appropriate extremity by the blood flow of that extremity. Norepinephrine was infused into the right brachial and femoral arteries of the patients at doses of 0.02, 0.05, 0.1, 0.2, 0.3, 0.5, and 0.7 microgram/min. Resting forearm and calf vascular resistances were similar in both groups of patients. The norepinephrine dose-response curves showed that control patients required more than three times the norepinephrine to produce the same percent increase in forearm vascular resistance (after 0.2 microgram/min forearm vascular resistance increased by 55% in the coarctation group, while the resistance in the control group increased by only 3%, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased forearm vascular reactivity in patients with hypertension after repair of coarctation. 397 23

This study characterizes a cellular mechanism for oscillatory contractions induced by norepinephrine in vascular smooth muscle from spontaneously hypertensive stroke prone rats (SHRSP). Helically cut strips of tail arteries from SHRSP and normotensive Wistar-Kyoto rats (WKY) were mounted in a muscle bath for measurement of isometric force generation. Norepinephrine-induced responses of arteries from SHRSP were characterized by fluctuations in contractile activity, whereas those in arteries from WKY remained constant with time. The magnitude of the oscillatory contractile activity (frequency X mean amplitude) varied directly with norepinephrine concentration (5.9 X 10(-9) to 1.8 X 10(-7) M). The oscillatory contractile activity varied inversely with the potassium concentration (3-20 mM) of the buffer solution and directly with the calcium concentration (0.1-5.0 mM) of the buffer solution. The oscillatory activity was converted to maintained contraction by barium (10(-4) M), quinidine (3 X 10(-6) M), sparteine (10(-3) M), D-600 (10(-7) M), and nifedipine (10(-8) M). Tetraethylammonium and 3,4-diaminopyridine, inhibitors of voltage-dependent potassium channels, did not alter the oscillatory contractile activity induced by norepinephrine. These observations suggest that oscillatory contractile activity in tail arteries from SHRSP is caused by an abnormal variation in potassium efflux during stimulation with norepinephrine. The altered potassium efflux appears to be related to calcium entry, which is sensitive to inhibition by channel blockers. This altered membrane property may contribute to changes in vascular sensitivity in hypertension.
Hypertension
PMID:Oscillatory contractions in tail arteries from genetically hypertensive rats. 399 33

The influence of age, sex and hypertension on urinary excretion of free catecholamines was evaluated in 190 men (64 hypertensive patients) and 75 women (10 hypertensive patients). Noradrenaline correlates positively with age in healthy men (r = 0.37, p less than 0.001) and women (r = 0.36, p less than 0.001). Adrenaline and dopamine do not show any significant correlation with age. Noradrenaline excretion is slightly higher in young (less than or equal to 39 years of age) and significantly higher in old (greater than or equal to 40 years of age) hypertensive patients than in age-matched control subjects. Noradrenaline (32 +/- 15 micrograms X 24 h-1) and adrenaline excretion (9 +/- 7 micrograms X 24 h-1) are lower in the group of younger women than in younger men (52 +/- 23 and 19 +/- 12 micrograms X 24 h-1). We assume that the lower excretion of free catecholamines in younger women is significant for a lower sympathetic activity.
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PMID:[Excretion of free catecholamines in relation to age, sex and blood pressure]. 401 64

Sympatho-adrenal and cardiovascular reactivity was studied in patients with pregnancy-induced hypertension (PIH) and healthy pregnant controls subjected to an isometric handgrip test and a cold pressor test both during and after the pregnancy. At rest, heart rate was higher in the PIH group than in the control group both during and after pregnancy. Forearm vascular resistance was not affected by PIH or by pregnancy per se. During pregnancy arterial plasma adrenaline levels were suppressed in the control group both when compared with the PIH group and postpartum values. Arterial noradrenaline levels were similar and normal in the two groups at both examinations. The isometric exercise increased systolic and diastolic blood pressures, heart rate and noradrenaline and reduced vascular resistance similarly in the PIH and control groups on both occasions. Vasoconstrictor responses to the cold pressor test were reduced during pregnancy but there were no differences between the groups on either occasion. Noradrenaline responses to the cold pressor test were not influenced by PIH or by pregnancy per se. During pregnancy adrenaline responses to the two tests tended to be reduced in the controls but not in PIH. Our results indicate enhanced adrenomedullary activity in PIH when compared with the suppressed activity in normal pregnancy. Cardiovascular reactivity to the tests was similar in the PIH and control groups. The normal arterial noradrenaline levels at rest and during provocation do not support the contention of a generalized increase in sympathetic nerve activity in PIH.
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PMID:Sympatho-adrenal and cardiovascular reactivity in pregnancy-induced hypertension. I. Responses to isometric exercise and a cold pressor test. 401 33

1. Twenty-four hours after the last of 4 intravenous doses of 6-hydroxydopamine (2x50 mg/kg on day 1 and 2x100 mg/kg on day 7) a complete impairment of adrenergic nerve function was observed in various organs of the rat.2. A complete recovery of adrenergic nerve function in vascular smooth muscle was observed 7 days after the last dose of 6-hydroxydopamine whilst in non-vascular smooth muscle recovery took between 14 and 21 days.3. On day 8, noradrenaline depletion produced by 6-hydroxydopamine was not as great in vascular tissues, such as the mesentery and renal artery, as in other tissues, such as the heart and salivary glands. Noradrenaline concentrations recovered much more rapidly in vascular than in other tissues.4. Electron microscope studies of small mesenteric arteries showed a complete destruction of adrenergic nerve terminals 24 h after 6-hydroxydopamine (2x100 mg/kg). However, there was a reappearance of growing terminals within 7 days and after 28 days the regrowth of adrenergic nerve terminals seemed complete.5. From the morphological and functional data it is concluded that 6-hydroxydopamine does produce complete destruction of vascular adrenergic nerve terminals. However, these terminals regenerate more rapidly than those in other tissues. This could explain the failure of intravenously administered 6-hydroxydopamine to prevent the development of experimental hypertension in the rat.
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PMID:Rapid recovery of vascular adrenergic nerves in the rat after chemical sympathectomy with 6-hydroxydopamine. 472 94

Two patients with severe postural hypotension associated with upper motor neuron and cerebellar impairment (Shy-Drager syndrome) have been studied. Head-up tilt and lower body negative pressure application caused marked falls in arterial pressure; in one patient, paradoxical vasodilatation was observed. Ice application did not increase arterial pressure or calculated forearm vascular resistance. Intravenous atropine in one patient increased heart rate by 18 beats per min, a cardioacceleratory response similar to exhausting recumbent exercise in that patient. 24 hr urinary catecholamine excretion was low, but aldosterone secretory rate was normal in the more severely afflicted patient. A prolonged elevation of plasma renin activity was noted when post-tilt hypertension occurred. When head-up tilt was not followed by this hypertensive period, plasma renin activity response to tilting was normal. Intra-arterial norepinephrine and tyramine both elicited a vasoconstrictor response. Intra-arterial infusions of norepinephrine and tyramine were repeated after administration of the monoamine oxidase inhibitor tranylcypromine. Norepinephrine was potentiated 4.1- and 0.5-fold in the two patients; tyramine was potentiated 3.7-and 1.1-fold in the two patients, respectively. A therapeutic program of tranylcypromine and tyramine (in the form of cheddar cheese) resulted in substantial clinical improvement. It is concluded that in at least some patients with idiopathic postural hypotension, norepinephrine is present in postganglionic sympathetic fibers. A therapeutic program of tyramine and a monoamine oxidase inhibitor may be of value when more conventional modes of therapy fail.
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PMID:Idiopathic postural hypotension: physiologic observations and report of a new mode of therapy. 543 69

The role of renal nerves in influencing the control of arterial pressure was studied in Wistar rats with aortic depressor nerve (ADN) transection. Renal denervation prevented or reversed the normal increase in arterial pressure seen after ADN transection. This effect was not due to an effect on the renin-angiotensin system, as the elevated arterial pressure after ADN section in rats with renal nerves intact was shown to be due to increased alpha-adrenergic activity. Food and water intake and urine output decreased significantly in both renal-denervated and sham-denervated rats after ADN section, suggesting that a pressure diuresis mechanism was not responsible for preventing the rise in pressure in renal-denervated rats. In another study, the concentration of norepinephrine in skeletal muscle and hypothalamus at 0 and 8 hours after inhibition of tyrosine hydroxylase with alpha-methyltyrosine was used as an index of norepinephrine turnover. Norepinephrine turnover in skeletal muscle was increased significantly over control values by ADN transection in sham renal-denervated rats, but was not significantly different from controls in renal-denervated rats with ADN section. In the hypothalamus, there was a significant difference between the turnover of norepinephrine in the two groups of ADN-sectioned rats. The results taken together suggest that renal denervation prevents the arterial pressure response to ADN transection by altering the central mechanisms governing sympathetic outflow. It is suggested that this effect may be due to elimination of information carried by afferent renal fibers.
Hypertension
PMID:Effect of renal denervation on arterial pressure in rats with aortic nerve transection. 613 68


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