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

Sympathetic-adrenal medullary hyperreactivity to acute stress, measured as an exaggerated elevation of plasma epinephrine and norepinephrine levels in response to footshock, was examined in four genetically related, inbred rat strains, all derived from the Wistar-Kyoto rat (WKY). These four strains are endowed with the traits of hypertension and behavioral hyperactivity, expressed either together (in SHR), or separately in two new strains (Wistar-Kyoto hyperactive rats, WK-HA, and Wistar-Kyoto hypertensive rats, WK-HT), or not at all (in WKY). Male rats of the SHR, WKY, WK-HA and WK-HT strains were subjected to acute footshock stress in order to determine whether the previously reported hyperreactivity of the SHR is attributable to the hypertensive trait, or to the behavioral hyperactivity trait, both of which are characteristic of the SHR. Plasma catecholamine levels were determined prior to, immediately following, and 5 min following acute footshock stress. We report here that the WK-HA strain (hyperactive but not hypertensive) exhibited the hyperreactivity characteristic of SHRs, and not the WK-HT strain (hypertensive but not hyperactive). We conclude that the exaggerated sympathetic-adrenal medullary response to acute stress is associated with the hyperactivity trait and not with hypertension among these congenic rat strains.
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PMID:Sympathetic-adrenal medullary response to stress in hyperactive and hypertensive rats. 323 14

Cardiovascular and behavioural responses to alerting stimuli (100 ms air puff) are exaggerated in spontaneously hypertensive rats (SHR). Wistar-Kyoto rats (WKY) exhibit bradycardia accompanying a startle-induced pressor response, whereas SHR demonstrate tachycardia. This study was designed to determine whether hyper-responsivity to startle is genetically linked to hypertension in SHR. An F1-generation, bred from SHR males and WKY females, demonstrated motor and cardiovascular responsiveness not different from WKY parents. Brother-sister mating of F1-animals produced an F2-generation with widely distributed blood pressures. Segregation of F2 by systolic blood pressure (greater than 180 or less than 180 mmHg) produced a 1:3 distribution. Neither group showed abnormal motor or pressor responses to startle. However, the F2 group with elevated arterial pressure exhibited tachycardia to startle that was similar to SHR grandparents. The heart rate response to acute stress may therefore serve as a more reliable genetic marker for hypertension than either the behavioural or blood pressure response, and apparently shares close genetic linkage with the hypertension.
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PMID:Genetic transmission of hyper-responsivity in crosses between spontaneously hypertensive and Wistar-Kyoto rats. 324 Dec 48

Age-related changes in circulatory responses to short-term shaker stress were investigated in conscious spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Hemodynamics (microspheres) were measured at 8, 24, 48, and 96 weeks of age, and plasma catecholamines were measured at 8 and 96 weeks. At rest, elevated mean arterial pressure was associated with unaltered cardiac index and heart rate in SHR compared with WKY at all ages. Regional blood flow was largely similar in both strains, except for a reduced renal flow in 96-week-old SHR. Cardiac index and most regional blood flow tended to or did decline in both strains between 8 and 96 weeks. Plasma catecholamines were similar in both strains at 8 and 96 weeks. Shaker stress evoked responses similar to defense reactions in both strains. The incremental responses in mean arterial pressure, heart rate, cardiac index, and cerebral, skeletal muscle, and myocardial flow and the decremental responses in splanchnic, renal, and skin flow were greater in SHR than in WKY, particularly at 8 weeks. Most of these responses tended to or did decline between 8 and 96 weeks in both strains. The plasma catecholamine responses were also greater in SHR at 8 and 96 weeks, and they did not differ in either strain between these ages. Thus, circulatory and sympathoadrenal reactivity to acute stress were enhanced in SHR compared with WKY, independently of age.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Apr
PMID:Cardiovascular responses to acute stress in young-to-old spontaneously hypertensive rats. 355 2

The radioactive microsphere technique was used to study hemodynamic mechanisms of action of 2 calcium antagonists--foridon and nifedipine in conscious rabbits with acute hypertension evoked by immobilization. Microspheres were injected before and 5 min after bolus i.v. injection of equihypotensive (10% blood pressure drop) doses of nifedipine (30 mcg/kg) and foridon (50 mcg/kg). Nifedipine in most cases decreased cardiac index by 7% without significant changes in regional hemodynamic. After foridon injection total peripheral resistance decreased by 19% (P less than 0.05) and cardiac index increased by 18%. There were increase in blood flow: in the heart by 34% (P less than 0.05), in the skeletal muscle by 41% (P less than 0.05) and in testes by 12% (P less than 0.05). The results show that in acute stress-induced hypertension these dihydropyridine-derivatives have different hemodynamic mechanisms of action: nifedipine preferentially depress myocardial contractility, whereas foridon dilates blood vessels.
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PMID:[Hemodynamic mechanisms of the hypotensive action of the new calcium antagonist foridon in acute hypertension in rabbits. A comparison with nifedipine]. 380 Nov 31

Epinephrine has been implicated in the genesis of some forms of hypertension. We have investigated the effects of epinephrine on vasoconstrictor responses evoked by adrenergic stimuli in the isolated perfused rat kidney. Low concentrations of epinephrine (2.5 - 5 X 10(-9) M) increased the amplitude of vasoconstrictor responses evoked by electrical stimulation of the renal adrenergic nerves. These concentrations of epinephrine had no effect on the basal perfusion pressure of the kidney or on the amplitude of vasoconstrictor responses evoked by exogenous norepinephrine. The potentiating effect of epinephrine persisted after infusion of the amine had ceased. Kidneys that had been perfused with 3H-epinephrine accumulated radioactivity, which could then be released by renal nerve stimulation. Cocaine (3 X 10(-5) M) reduced the renal accumulation of 3H-epinephrine and abolished both the persistent potentiating effect of the amine and the release of radioactivity evoked by subsequent nerve stimulation. The potentiating effect of epinephrine infusion was abolished by the beta 2-selective adrenergic receptor antagonist ICI 118,551 (3 X 10(-8) M), but not by the beta 1-selective adrenergic receptor antagonist atenolol (10(-6) M). These results indicate that concentrations of epinephrine that can be achieved during acute stress can enhance the amplitude of neurogenic vasoconstrictor responses. This effect appears to be mediated via a prejunctional beta 2-adrenergic receptor. The persistent nature of this effect may be due to the neuronal accumulation and subsequent release of epinephrine.
Hypertension
PMID:Epinephrine enhances neurogenic vasoconstriction in the rat perfused kidney. 398 58

Basing on the hypothesis that disturbances of cerebral information processing on the basis of acute or chronic stress situations or profound neurotic alterations are being directed to the cardiovascular system only by predisposition to hyperreactivity, the influence of a psycho-nervous-humoral-hormonal stepped load schedule upon central nervous and vegetative functions was studied in baboons. Stochastic interventions into the natural day-night rhythm and application of NaCl and DOCA doses not per se causing a blood pressure rise, either single or in combination for altogether 3 years were used as disturbing factors. It has been revealed that experimental disturbance of the light-dark phases led to lasting deviations of the conditional-reflectory activity in the sense of a predominance of irritation processes. With motor response time, initially unchanged but from the second year of experiment significantly shortened by 35%, the failure rates at differentiation increased, on the average, from 6 to 45% and the intersignal responses by 100%. Even after exposure for several months, no disorders of the cardiovascular system occurred. It was only the coupling with an experimentally induced disturbance of electrolyte distribution that provoked a significant increase in mean arterial pressure, on the average, by 24% of the pre-control value with moderate increase of the circulating blood volume. The increases in free fatty acids and blood glucose concentrations by 14 and 23%, respectively, can be interpreted as additional hypertension-favouring factors. Despite an application of mineral corticoids for more than 1 year, it has been impossible to alter the contraction behaviour of the vascular smooth muscle cell in the sense of an experimentally induced predisposition to arteriolar hyperreactivity outlasting the discontinuation of disturbing factors. With higher nervous activity being clearly disturbed as before, the pressure got back to normal; testing the vascular reactivity to noradrenaline (1.0 microgram/kg b.w/min i.v., for 5 min) or angiotensin II (0.5 microgram/kg b.w. i.v.) at the end of the investigation period gave no enhanced pressure responses. By contrast, animals exposed exclusively to the described combination load for 18 weeks, showed a still normal system pressure and sensitivity to the applied noradrenaline and angiotensin II increased by 75-120% of the pre-control response. A liability of the cardiovascular system at acute stress situations (multiple partial immobilization) in long-term neurotically predamaged monkeys in the 24-h experiment was impressive by a cardiodepression during the nightly regeneration phase, reduced on the average by 35 beats/min against the control group. Thus, our results support the hypothesis of a cerebro-visceral pathoconstellation as the etiological principle of certain forms of the inhomogeneous clinical picture of primary hypertension.
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PMID:[Arterial hypertensive dysregulations on the basis of a cerebro-visceral stimulus constellation in baboons]. 712 52

Combined effects of prazepam and trichlormethiazide (TCM) which were given simultaneously were studied in renal hypertensive rats (1-kidney type) and DOCA hypertensive rats. In this study the blood pressure was measured by the plethysmographic method. Orally administered prazepam alone did not show any appreciable effect on the blood pressure, while TCM, even when administered alone, exhibited marked and long-lasting hypotensive effects of both hypertensive rats. In addition, the hypotensive effect of TCM was apparently potentiated by the concurrent use of prazepam. In the experiment where conscious and unconstricted spontaneous hypertensive rats (SHR) were used, the pressor response and tachycardia were observed when foot shock (acute stress) was loaded. This pressor response was the "all or none" type and a threshold existed. In contrast to the pressor response, the degree of tachycardia varied depending on the intensity of the stress. The similar responses were also observed in normotensive rats, although the degrees of the responses were significantly weaker than those in SHR. Prazepam given alone obviously suppressed the cardiovascular responses mentioned above. The present results suggest that prazepam is an useful drug for the treatment of hypertension.
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PMID:[Effect of prazepam on experimental hypertensive models]. 712 44

Lungs of 20 rats flown aboard Cosmos-936 for 18.5 days and sacrificed within 5-13 hours (8 weightless and 4 centrifuged rats) and 25 days (4 weightless and 4 centrifuged rats) after recovery were studied histologically. An identical number of lung specimens were withdrawn from rats of synchronous and vivarium controls. Lungs of the flight rats did not show any pathological changes or morphological signs of prolonged congestion, thus indicating the lack of hypertension in pulmonary circulation. Lungs of the flight rats exhibited an increased leukocyte count, which was more marked in the weightless rats killed 8-13 hours postflight. The elevation in the count of neutrophilic leukocytes in the flight rats was due to peripheral neutrophilia which is a manifestation of an acute stress-reaction. An exposure of rats to artificial gravity was responsible for a lesser increase in the count of neutrophilic leukocytes.
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PMID:[Morphologic changes in the lungs of rats after a flight aboard biosatellite "Cosmos-936"]. 742 Oct 97

Recent observations demonstrate the presence of neurosteroids and their rapid increase in response to acute stress. In view of a steroidal nature of ouabainlike compound, we tested the hypothesis that ouabainlike compound may participate in a homeostatic response to acute stress. Male Wistar rats were subjected to acute stress by swimming in water (22 degrees C) for 10 minutes. The levels of ouabainlike compound in plasma, hypothalamus, pituitary, and adrenal at 10, 40, and 70 minutes (n = 8 for each) after the end of swim stress were compared with nonstressed control levels (n = 10). Ouabainlike compound was measured by a radioimmunoassay for ouabain. Plasma levels of corticosterone and catecholamines were also measured. Plasma corticosterone concentrations increased rapidly at 10 minutes (P < .01) and then declined. A trend for a rise in plasma catecholamines was found at 10 minutes. Adrenal levels of ouabainlike compound concomitantly increased at 10 minutes (P < .01, control: 58.9 +/- 5.9 pmol ouabain equivalents per gram; 10 minutes: 92.5 +/- 4.8; 40 minutes: 47.3 +/- 9.6; 70 minutes: 45.1 +/- 6.3). In contrast, the response of plasma ouabainlike compound was slow and doubled at 40 minutes (P < .01, control: 115 +/- 12 pmol ouabain equivalents per liter; 10 minutes: 132 +/- 23; 40 minutes: 226 +/- 53; 70 minutes: 117 +/- 16). Ouabainlike compound levels in hypothalamus and pituitary remained unaltered. These findings suggest that ouabainlike compound may function as a stress hormone.
Hypertension 1995 Dec
PMID:Stress-induced elevation of ouabainlike compound in rat plasma and adrenal. 749 90

The effects of two types of laboratory stressors, a structured interview and the cold pressor test, on blood pressure (BP) and heart rate (HR) were studied in normotensive individuals (n = 16), unmedicated hypertensive patients (n = 12), and medicated hypertensive patients (n = 46). Fifteen patients were in the bisoprolol group, 16 patients were in the enalapril group, and 15 patients were in the nitrendipine group. Concurrent physiologic measures, finger pulse volume (FPV), electrodermal activity, and respiratory frequency (RF), were also used to evaluate the level of stress reached by the subjects during and after the tasks. No significant differences were evident between the different treatments in BP and other physiologic responses to stressors. Patients receiving bisoprolol maintained lower HR and systolic BP values, but these differences were not related to the reaction to the stressors. No significant differences were noted in diastolic BP (DBP) between the different groups. The highest physiologic responses were obtained during the structured interview. Antihypertensive monotherapy does not attenuate cardiovascular reactions induced by acute stress in controlled laboratory conditions. In laboratory studies of the relationships between stress and hypertension, it is important that social stressors be used and that physiologic rather than cardiovascular measures of stress be recorded.
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PMID:Antihypertensive monotherapy and stress-induced changes in physiological activity. 767 64


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