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)

Dl-propranolol, acebutolol, atenolol, bupranolol, oxprenolol, pindolol, practolol, sotalol and d-propranolol were injected into the cisterna magna of anesthetized dogs with neurogenic hypertension induced by deafferentation and vagotomy. Dl-propranolol and bupranolol correct the hypertension and the tachycardia of the debuffered dog, whereas oxprenolol has only an action on the heart rate. The other beta-blocking drugs and d-propranolol were inactive at the doses used. Our results show that a mere central effect cannot explain the antihypertensive properties of all the tested beta-blocking agents.
 ...
PMID:Antihypertensive effects of intra-cisternal beta-blocking agents in dogs with acute nerogenic hypertension. 3 26

Renin activity (RA) in peripheral plasma, as well as in renal cortex and brain (cortex, stem and medulla) homogenates of rats with spontaneous, Goldblatt, NaCl, adrenal-regeneration and neurogenic hypertension was biologically assayed. The results suggest that RA exists not only in the brain of normotensive but of hypertensive rats as well. RA in the medulla is higher than in other brain areas and in the kidney, both in normotensive and in hypertensive rats with the exception of rats with adrenal regeneration and NaCl hypertension. In most of the experimental forms of hypertension (neurogenic, renal, spontaneous) in which RA in the medulla is increased, the role of the brain renin-angiotensin system seems to predominate, while in forms in which renal RA is elevated (adrenal regeneration) the kidney renin system most probably plays a more important role. A definite inverse interrelation between the brain and the kidney renin-angiotensin systems was established. The interrelation between the two renin systems in NaCl hypertension could not be evaluated, since exogenous factors (Na), which interfere with the kidney renin system, play a considerable role in the pathogenesis of NaCl hypertension.
 ...
PMID:Renin activity in the brain, the kidneys and the peripheral plasma or rats with different experimental models of hypertension. 59 8

Hemodynamic parameters and the Rorschach test were performed on 48 borderline and 64 sustained essential hypertensive patients, and compared with 33 normal subjects. Hemodynamic patterns suggested (1) in borderline hypertensives, a neurogenic hypertension, and (2) in sustained hypertensives, a volume- and renal-mediated hypertension. Repeat hemodynamic determinations were performed on 35 borderline hypertensives after a 47 +/- 3-month follow-up survey. The results confirmed that, in the same patient, hypertension was successively neurogenic and volume-mediated. The results of the Rorschach test in the overall hypertensive population pointed to an incapacity to form a structured neurosis because of the lack of a fantasy life, and an inadequacy of the mechanisms of repression of aggressive tendencies. These observations were more marked in sustained hypertensives. In borderline hypertensives, the lack of fantasy life, assessed from kinesthetic perceptions, was highly significant (p less than 0.01) and was associated with anxiety and functional symptoms suggesting an increased lability of the autonomic nervous system. In sustained hypertensives, however, there was an inability to express anxiety in a symbolic fashion (p less than 0.01). These differences in psychological findings between borderline and sustained hypertensives agree with the difference in hemodynamic patterns. The results suggest that sustained hypertensives have a predominantly somatic issue in place of the psychological conflicts observed in borderline hypertensives.
 ...
PMID:Hemodynamic factors and Rorschach testing in borderline and sustained hypertension. 74 6

1. Noradrenaline, adrenaline and alpha-methylnoradrenaline administration into the nucleus tractus solitarii (NTS) of anaesthetized rats decreased blood pressure and heart rate in a dose-dependent fashion. 2. Bilateral injections were effective in lower doses than unilateral administration. alpha-Methylnoradrenaline given bilaterally produced hypotension in a dose of 0-08 nmol whereas after unilateral injection a dose of 0-32 nmol was needed to obtain the same degree of hypotension. 3. Electrical stimulation of the NTS caused hypotension and bradycardia. Conversely, bilateral electrolytic lesions or deafferentation of the NTS led to acute hypertension. Chronically such lesions caused neurogenic hypertension. 4. In spontaneously hypertensive rats increased concentrations of noradrenaline, adrenaline and dopamine were measured in the part of the NTS located just caudal to the obex (A2 region).
 ...
PMID:Brain-stem structures and catecholamines in the control of arterial blood pressure in the rat. 79 55

Blood pressure, heart rate, and plasma catecholamine levels were measured in 16 quadriplegic subjects with physiologically complete cervical spinal cord transections above the level of the sympathetic outflow, and in 15 normal subjects (controls). In the quadriplegics the average resting blood pressure was 107/59 (mean, 75) mmHg, heart rate was 65 beats/min, and plasma norepinephrine (NE) and epinephrine (E) levels were 0.05 and 0.005 ng/ml, respectively. In the controls average resting blood pressure was 117/79 (mean, 92) mmHg, heart rate was 61 beats/min, and resting plasma NE and E levels were 0.20 and 0.06 ng/ml, respectively. Resting blood pressure and plasma NE and E levels were significantly lower in the quadriplegics (P less than 0.01, less than 0.001, less than 0.001, and less than 0.001, less than 0.001, respectively) than in the controls. In the quadriplegics, neurogenic hypertension was induced by bladder and muscle stimulation. This resulted in a marked elevation of both systolic and diastolic blood pressure (from an average of 109/60 (mean, 75) to 168/87 (mean, 114) mmHg) as a result of uninhibited sympathetic nervous activity through the isolated spinal cord. Plasma NE consistently rose, from an average of 0.05 to 0.16 ng/ml (P less than 0.001). There was significant linear relationship between plasma NE and mean blood pressure (P less than 0.001). In the quadriplegics infusion of l-norepinephrine to raise the blood pressure to comparable levels (from 105/58 (mean, 74) to 183/93 (mean, 123) mmHg) resulted in plasma NE levels approximately 21 times higher than during muscle and bladder stimulation. It is possible that the lower resting arterial blood pressure and plasma NE and E levels in the quadriplegics in comparison to normal subjects may reflect diminished resting sympathetic nervous activity. The rise in blood pressure following increased sympathetic nervous activity was accompanied by an elevation in plasma NE. The hypertension was not secondary to the rise in plasma NE. Plasma NE in these subjects appears to be a reliable index of prevailing sympathetic nervous activity.
 ...
PMID:Plasma catecholamines during paroxysmal neurogenic hypertension in quadriplegic man. 93 5

Electrical stimulation of the posterior hypothalamus is followed by an immediate increase in sympathetic nerve activity and rise in blood pressure. Destruction of hypothalamic adrenergic structures by local unilateral injection of 6-hydroxydopamine into the posterior hypothalamus reduced the blood pressure rise in response to stimulation of the lesioned side. This and numerous other findings indicate an involvement of central adrenergic neurons in the mediation of an increase of sympathetic nerve activity caused by hypothalamic stimulation. However, central adrenergic neurons do not seem to be an integral part of the sympathoexcitatory pathways originating in the posterior hypothalamus but rather facilitate their activation: after almost complete norepinephrine depletion produced by combined treatment with reserpine and alpha-methl-p-tyrosine, hypothalamic stimulation was still followed by an increase in spontaneous sympathetic nerve activity. Stimulation of an alpha-adrenoceptive site, probably located in the lower brain stem, mimics an activation of the baroreceptor reflex. The hypotensive drug, clonidine, stimulates this alpha-adrenoceptive site. In low doses clonidine facilitates the activation of the reflex, and in high doses this drug induces a state which closely resembles a pronounced activation of the reflex. Experiments following depletion of norepinephrine suggest that the central part of the baroreceptor reflex arc does not contain adrenergic neurons. However, these findings are compatible with the view that some neurons within the reflex arc are supplied with alpha-adrenoceptors. For the present it cannot be stated with certainty whether these alpha-adrenoceptors possess an innervation by adrenergic neurons projecting onto the reflex arc. In favor of such an innervation are the obsevations that alpha-methyldopa has its site of action in the lower brain stem and that the integrity of central adrenergic neurons is essential for its hypotensive effect. It seems that two central adrenergic systems exist with opposing effects on cardiovascular control. These are an excitatory hypothalamic and an inhibitory bulbar adrenergic system. Partial destruction of central adrenergic neurons by intraventricularly injected 6-hydroxydopamine prevents the development of DOCA/NaCl, renal, and neurogenic hypertension and alters the pattern of blood pressure rise in spontaneously hypertensive rats. Impairment of central adrenergic function or imbalance of the two central adrenergic mechanisms may represent a trigger mechanism for the initiation of hypertension.
 ...
PMID:Cardiovascular regulation by central adrenergic mechanisms and its alteration by hypotensive drugs. 109 54

1. Arterial blood pressure and heart rate were measured before, during and after cutaneous and visceral stimulation in subjects tetraplegic due to severe cervical spinal cord damage. Stimulation resulted in marked hypertension as a result of reflex sympathetic overactivity. 2. Mixed venous blood from a catheter situated in the right atrium was obtained before and after stimulation and plasma prostaglandin E and prostaglandin F were measured. A consistent and significant rise in plasma prostaglandin E, but not plasma prostaglandin F, accompanied the hypertension. 3. It is suggested that prostaglan ding E is released during this sympathetic nervous activity and may be related to neurogenic hypertension.
 ...
PMID:Plasma prostaglandin E during neurogenic hypertension in tetraplegic man. 120 95

1. The effect of (R)-alpha-methylhistamine, a selective H3-histamine receptor agonist, was examined on the neurogenic hypertension and tachycardia that is induced by stimulation of areas in the medulla oblongata of guinea-pigs. Electrical medullary stimulation (32 Hz, 3-5 s trains, 0.5-1.0 ms square pulse, 25-400 microA) produced intensity-dependent increases in blood pressure and a more variable tachycardia. 2. (R)-alpha-methylhistamine inhibited the hypertension and tachycardia due to submaximal CNS stimulation. The inhibition of hypertension by (R)-alpha-methylhistamine was dose-dependent (10-300 micrograms kg-1, i.v.) and was not seen at high intensities of stimulation. 3. (R)-alpha-methylhistamine (300 micrograms kg-1, i.v.) did not attenuate the pressor response to adrenaline (1 and 3 micrograms kg-1, i.v.), indicating that the effect of (R)-alpha-methylhistamine was not mediated by a postjunctional action on smooth muscle. 4. The inhibition of CNS-induced hypertension by (R)-alpha-methylhistamine (300 micrograms kg-1, i.v.) was blocked by the H3 antagonists, thioperamide (ID50 = 0.39 mg kg-1, i.v.), impromidine (ID50 = 0.22 mg kg-1, i.v.) and burimamide (ID50 = 6 mg kg-1, i.v.). The rank order potency of these antagonists is consistent with activity at the H3B receptor subtype. Chlorpheniramine (30 micrograms kg-1, i.v.) and cimetidine (3 mg kg-1, i.v.) did not antagonize the inhibition of CNS-hypertension by (R)-alpha-methylhistamine. 5. These results suggest that (R)-alpha-methylhistamine inhibits sympathetic hypertensive responses in guinea-pigs by activation of prejunctional H3-receptors, possibly located on postganglionic nerve terminals. Furthermore, on the basis of the rank order potency to different H3-antagonists, it appears that the H3B-receptor subtype is involved with H3-receptor responses on vascular sympathetic nerves.
 ...
PMID:Inhibition of sympathetic hypertensive responses in the guinea-pig by prejunctional histamine H3-receptors. 133 Jan 74

Several authors have discussed an alteration of adrenergic receptivity in arterial hypertension. De Champlain (Hypertension 1990; 8: S77-S85) suggested that postsynaptic alpha 1-adrenergic functions became dominant while beta-adrenergic functions are attenuated in arterial hypertension. However, the status of presynaptic alpha 2-adrenoceptors remains unknown. The present study investigates presynaptic alpha 2-adrenoceptors in hypertension through the measurement of plasma levels of noradrenaline after administration of yohimbine, an alpha 2-adrenoceptor antagonist, in essential hypertension. Yohimbine (0.2 mg/kg per os) induced a 73% increase of plasma levels of noradrenaline in hypertensive patients (n = 12) and a 178% one in normotensive subjects (n = 6, p < 0.05). A similar significant difference was found in experimental neurogenic hypertension observed in awake dogs 3 weeks after sinoaortic denervation: the increase in plasma concentrations of noradrenaline after yohimbine (0.5 mg/kg i.v.) was +279% in hypertensive versus +642% in normotensive dogs (p < 0.05). The results show that the magnitude of the yohimbine-induced sympathetic activation is lower in hypertensives than in normotensives. They suggest the existence of a presynaptic alpha 2-adrenoceptor desensitization in arterial hypertension. The abnormality of this presynaptic inhibitory mechanism can increase the sympathetic tone and help to develop and maintain arterial hypertension.
 ...
PMID:[Is there any desensitization of presynaptic alpha 2-adrenergic receptors in hypertension? Experimental and clinical studies]. 136 44

Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. Excessive vasoconstriction resulting from noradrenaline (norepinephrine) in neurogenic hypertension, phaeochromocytoma, orthostatic hypertension and alpha-adrenergic drug administration; angiotensin excess due to renal ischaemia brought about by aortic coarctation, renal arterial and arteriolar stenosis, intraluminal obstruction, external renal compression, renin-producing tumours, intrinsic kidney diseases and excessive renin substrate; and vascular structural disorders such as atherosclerosis, arteriolitides and fibrosis with or without calcification of major arteries may also induce hypertension. Secondary hypertension of uncertain mechanism may occur in hyperparathyroidism, hyper-or hypothyroidism, or acromegaly. All are best treated by appropriate correction of the endocrine excess or deficiency. It may also occur in pregnancy, where the mechanism may involve prostaglandin-thromboxane imbalance or calcium deficiency; calcium deficiency with some evidence of benefit from calcium supplements; and the recumbent hypertension paradoxically associated with autonomic failure. Excellent responses to specific correction of the underlying cause or pathogenetic mechanism is usual in young individuals but less frequent in older patients.
 ...
PMID:Secondary hypertension. An overview of its causes and management. 137 54


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