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

Cerebral hemispheric blood flow and metabolism were measured before and after therapy with intracarotid infusion of combined PBZ and PPL in 15 patients with recent cerebral infarction. HBF was unaltered despite decrease in cerebral perfusion pressure. Cerebral hemispheric oxygen comsumption and carbon dioxide production decreased while cerebral hemispheric lactate production increased. Biphasic cerebral uptake of tyrosine was observed during and immediately after PBZ and PPL infusion. CSF HVA increased, indicating altered DA turnover. CSF 5HIAA levels also increased, suggesting altered 5HT turnover after PBZ and PPL. Release of cyclic AMP from ischemic brain into cerebral venous blood seen in the steady state was abolished after therapy. Cerebral hemodynamic studies suggest a functional balance between monaminergic neurogenic influences in the control of cerebral circulation. Imbalance of such controlling factors in ischemic brain may lead to paradoxical vascular responses to induced hypertension and hypotension. PBZ and PPL enhance such responses perhaps by increasing central neurotransmitter turnover and release. Further shift toward cerebral anaerobic metabolism may occur in ischemic brain following the use of phenoxybenzamine and propranolol. Worsening of neurological deficit occurred in four cases. Combined therapy with PBZ and PPL does not appear beneficial in the therapy of patients with recent stroke.
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PMID:Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients. 0 7

A 12-year-old boy with a norepinephrine-secreting pheochromocytoma that caused hypertension resistant to oral alpha adrenergic blockade is reported. Resistance to alpha adrenergic blocking agents developed when the patient's daily propranolol dosage was lowered from 10 to 1 mg/kg. Subsequently, alpha methyl tyrosine, an inhibitor of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, controlled the patient's blood pressure and was associated with reduction in total urinary catecholamine excretion. Norepinephrine content of the tumor and uninvolved adrenal gland removal at surgery was reduced. These findings confirm that alpha methyl tyrosine inhibited in vivo synthesis of catecholamines.
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PMID:Childhood pheochromocytoma: treatment with alpha methyl tyrosine for resistant hypertension. 1 59

High blood pressure in DOCA-saline treated uninephrectomised rats is prevented or even reversed by tyrosine, tyramine or by treatments which - based on circumstantial evidence - might increase local brain tyramine concentration.
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PMID:d-Tyrosine prevents hypertension in DOCA-saline treated uninephrectomised rats. 57 36

We describe a method for determining those urinary total phenolic compounds that are tyrosine analogs or metabolites, such as thyroxine and catecholamines. The urine sample, 4-aminoantipyrine in carbonate-bicarbonate buffer, and potassium ferricyanide solution are mixed and the quinoneimine dye that forms is measured at 500 nm. Some cases of hyperthyroidism, diabetes mellitus, nephrosis, obesity, hypertension, or catecholamine-producing tumor showed above-normal values, so that this determination seems useful as a screening test for these disorders.
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PMID:Determination of urinary total phenolic compounds with use of 4-aminoantipyrine: suggested screening test for hyperthyroidism and for catecholamine-producing tumor. 91 84

Prevention of high blood pressure in uninephrectomized, DOCA-saline treated rats was observed after treatment with central tyramine precursors. We suggest that the high blood pressure is either due to relative lack of tyrosine, which might be caused by the hyperactivity of tyrosine hydroxylase, or to hypoactivity of the decarboxylase: in both cases the result is diminished tyramine synthesis.
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PMID:Central tyramine prevents hypertension in uninephrectomized DOCA-saline treated rats. 92 98

Turnover of noradrenaline (NA) and dopamine (DA) in some regions of the rat brain was determined after 1 and 3 weeks of daily injections of lysine vasopressin (LVP) and 2 weeks after the termination of 28-day LVP injections. Disappearance of 3H-DA was estimated in the hemispheres, brain stem and striatum and of 3H-NA in the hemispheres and brain stem after intraventricular injection of 3H-tyrosine. A significant acceleration of 3H-NA disappearance from the hemispheres was found in all the experimental animals and from the brain stem 3 weeks after LVP adminstration and 2 weeks after its withdrawal. No marked changes in dopamine turnover in the examined regions of the rat brain were found. Since prolonged vasopressin administration produces hypertension in the rat it seems likely that central NA, but not DA, plays a role in the vasopressin-induced hypertension.
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PMID:Turnover of catecholamines in some regions of the rat brain during prolonged vasopressin administration and after its withdrawal. 94 87

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.
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PMID:Cardiovascular regulation by central adrenergic mechanisms and its alteration by hypotensive drugs. 109 54

The spontaneous hypertensive rat is an animal model characterized by a syndrome of hypertension, insulin resistance and hyperinsulinaemia. To elucidate whether in analogy to other insulin resistant animal models an inactivity of the insulin receptor kinase or an alteration of the glucose transporter (GLUT 4) level in the skeletal muscle might contribute to the pathogenesis of insulin resistance we determined insulin receptor kinase activity and GLUT 4 level in the hindlimbs of spontaneous hypertensive rats and normotensive control rats. Normotensive normoinsulinaemic Lewis and Wistar rats were used as insulin sensitive controls, obese Zucker rats were used as an insulin resistant control with known reduced skeletal muscle insulin receptor kinase activity. Binding of 125I-insulin, crosslinking of 125I-B26-insulin, autophosphorylation in vitro with 32P-ATP and phosphorylation of the synthetic substrate Poly (Glu 4: Tyr 1) were performed after partial purification of solubilized receptors on wheat germ agglutinin columns. GLUT 4 levels were determined by Western blotting of subcellular muscle membranes. Insulin receptors from spontaneous hypertensive rats compared to those from Lewis and Wistar rats showed no difference of the binding characteristics or the in vitro auto- and substrate phosphorylation activity of the receptor, while in the Zucker rats the earlier described insulin receptor kinase defect was clearly evident. Western blots of subcellular muscle membrane fractions with antibodies against GLUT 4 revealed no difference in transporter levels. These data suggest that insulin resistance in spontaneous hypertensive rats is caused neither by an insulin receptor inactivity nor by a decreased number of glucose transporters in the skeletal muscle.
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PMID:Normal insulin receptor tyrosine kinase activity and glucose transporter (GLUT 4) levels in the skeletal muscle of hyperinsulinaemic hypertensive rats. 132 60

To clarify the role of the renal and hypothalamic noradrenergic systems in the antihypertensive actions of dietary potassium supplementation in salt-loaded spontaneously hypertensive rats (SHR), we measured systolic blood pressure and norepinephrine turnover, which was determined from the rate of decline of tissue norepinephrine concentration after the administration of alpha-methyl-p-tyrosine, in 5-week-old SHR or age-matched Wistar-Kyoto (WKY) rats eating normal-NaCl (0.66%) or high-NaCl (8%) diet with supplementation of 8% KCl. In WKY rats, neither high-sodium nor high-potassium diets had an effect on blood pressure with no change in renal or hypothalamic norepinephrine turnover. In SHR, however, salt loading accelerated the development of hypertension. Potassium supplementation did not affect blood pressure in normal-sodium SHR but attenuated the rise in blood pressure with salt loads. Correspondingly, renal norepinephrine turnover in SHR was increased compared with that of WKY rats, and salt loading further potentiated the increased turnover in the kidney; however, no changes in hypothalamic turnover occurred. Potassium supplementation attenuated the rise in blood pressure with salt loads and the increased renal turnover. Stimulation of sympathetic discharge by cold exposure after the administration of alpha-methyl-p-tyrosine produced marked depletion of norepinephrine in most tissues. The loss of norepinephrine was significantly greater in both kidney and hypothalamus of salt-loaded SHR than in those of normal-sodium SHR, but potassium could normalize this. Thus, potassium not only diminished the increased renal norepinephrine turnover in the kidney under normal conditions but also attenuated the augmented renal and hypothalamic norepinephrine turnover by cold stress in salt-loaded SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Oct
PMID:Role of hypothalamic-renal noradrenergic systems in hypotensive action of potassium. 135 21

This article reports on the binding and the angiotensin II (Ang II) antagonistic properties of a peptide, referred to as hIIA, encoded by an RNA strand complementary to the human Ang II messenger RNA. Although Ang II and hIIA (H2N-Glu-Gly-Val-Tyr-Val-His-Pro-Val-COOH) share four amino acids, the iodinated and tritiated forms of hIIA were unreactive with seven monoclonal antibodies defining four distinct epitopes on the Ang II molecule and failed to bind to Ang II hepatic and mesangial receptors. However, hIIA did inhibit binding of 125I-Ang II to rat hepatocyte membranes (IC50, 2 x 10(-7) M) and to the various monoclonal antibodies. The lowest IC50 (5 x 10(-7) M) was measured with the monoclonal antibody specific for the Ang II sequence generally considered as implicated in receptor recognition. As predicted from the binding studies, hIIA was further shown to antagonize some biological properties of Ang II. On mesangial cells, hIIA alone had no effect on intracellular calcium concentration ([Ca2+]i) and prostaglandin E2 synthesis but did abolish the transient increase in [Ca2+]i in response to 100 nM Ang II and did induce a specific dose-dependent inhibition of the Ang II-stimulated prostaglandin E2 release. Furthermore, intravenous infusion of hIIA (200 micrograms.kg-1.min-1) inhibited by 66 +/- 3% the rat hypertensive response to 100 ng.kg-1 Ang II but had no effect on the pressor activity of agents such as alpha 1-adrenergic and HT2 serotonin agonists. Our data suggest that the "complementary" peptide hIIA interacts directly with Ang II by mimicking the Ang II complementary site on the receptor and can inhibit the physiological effects of Ang II. This type of Ang II complementary peptide may serve as a model for a new class of antihypertensive drugs.
Hypertension 1992 Apr
PMID:Antagonist effect of a receptor-mimicking peptide encoded by human angiotensin II complementary RNA. 155 66


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