Gene/Protein Disease Symptom Drug Enzyme Compound
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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

1. Dibutyryl cyclic AMP (Db cAMP, 75-500 microgram/kg), injected into the lateral ventricle of the brain of the cat increased blood pressure, heart rate and splanchnic discharge rate. 2. ATP, but not AMP, induced similar changes; GMP in small doses increased blood pressure. 3. A number of drugs are known to activate adenylate cyclase-induced hypertension, tachycardia and increase splanchnic discharge rate. This was shown for TRH, tetracosactide and a new beta2-adrenoceptor stimulant, NAB 365. 4. Injection into the lateral ventricle of theophylline or Ro 7/2956, both inhibitors of phosphodiesterase, similarly increased blood pressure. 5. Histamine administered by the same route induced similar reactions; it is not known if this action was exerted by activation of H1- or H2-receptors. 6. Somatostatin, known to reduce cAMP levels, induced a small but significant decrease in blood pressure. Melanocyte stimulating hormone release inhibiting factor (MIF) and TSH were ineffective. 7. These results provide evidence for the possibility of a role for cAMP in the central regulation of blood pressure at suprabulbar levels.
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PMID:Cyclic 3'5'-adenosine monophosphate and central circulatory control in cats and dogs. 2 Feb 56

Insulin-induced hypoglycemia previously has been shown to provoke a beta-adrenergic response that normally results in an increase in plasma renin activity (PRA). In our study, hypoglycemia induced definite increases in PRA in a group of five patients with normal renin essential hypertension but failed to do so in a group of six patients with low renin essential hypertension. In both groups, plasma cyclic adenosine 3',5'-monophosphate (cyclic AMP; cAMP) increased more than 2-fold during hypoglycemia, but the response in the low renin group was significantly less than that previously observed in normal subjects under the same conditions. Plasma cortisol increased to an equal extent in both groups of hypertensive patients during hypoglycemia. Infusion of the phosphodiesterase inhibitor, theophylline, resulted in definite increases of PRA in patients with normal renin hypertension but not in patients with low renin hypertension. Because changes in the level of plasma cAMP during hypoglycemia have been thought to reflect adrenal catecholamine release, our finding of a blunted increase in plasma cAMP during hypoglycemia in patients with low renin hypertension may suggest that there is a generalized alteration in adrenergic responsiveness in this condition.
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PMID:Contrasting effects of hypoglycemia on plasma renin activity and cyclic adenosine 3',5'-monophosphate (cyclic AMP) in low renin and normal renin essential hypertension. 17 76

The literature concerned with studies of the occurrence and function of the cyclic nucleotides in blood vessels is reviewed. Emphasis is placed on the critical evaluation of the evidence which relates to the hypothesis that cyclic nucleotides meditate the effects of drugs and neurotransmitters on vascular contractility. The hypothesis that cyclic AMP mediates vasodilation, especially that induced by beta-adrenergic relaxation, is supported by many experimental approaches, but it is concluded that the evidence remains unconvincing based on the criteria established for such a mediator role. Possible sites of action of cyclic AMP are discussed. The demonstrated action of cyclic AMP on vascular membrane electrophysiology and calcium ion pumps are reviewed as possible causes of relaxation. The role of both nucleotides in vascular disease, especially hypertension is discussed. Finally the needs for further research in this area are suggested.
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PMID:Occurrence and function of cyclic nucleotides in blood vessels. 17 65

Cyclic AMP levels and protein kinase activity were determined in the aortas of rats with normotension, moderate and severe spontaneous hypertension. While the cyclic AMP levels were reduced in the aortas from rats with moderate and sever hypertension the protein kinase levels were found to be elevated only in the aortas from rats with severe hypertension. We have grown in tissue culture, aortic smooth muscle cells from the normotensive and severely hypertensive rat. Cultured cells from both strains have similar growth patterns and morphology. The differences seen in cyclic AMP and protein kinase levels in the intact aortas are also seen in the aortic smooth muscle cells in cluture.
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PMID:Cyclic AMP and protein kinase in the spontaneously hypertensive rat aorta and tissue-cultured aortic smooth muscle cells. 18 60

Adenosine-3',5'-monophosphate (cyclic AMP) concentration was measured in plasma from nonpregnant women; women in the 7-41 weeks of normal pregnancy; during labor; and 5-7 h postpartum. The cyclic AMP levels in the course of normal pregnancy showed an initial peak volume at 14 weeks. After falling to nonpregnant level at 18 weeks, it began to rise steadily and reached a second peak at 34 weeks. A gradual decline was then followed until labor. The postpartum plasma concentration was significantly lower than the nonpregnant level. A similar pattern was found in serial studies in 4 women of normal pregnancy. Sequential cyclic AMP measurement in 5 hypertensive pregnancies showed a markedly elevated level during 16-26 weeks, but became comparable to normal pregnancy values thereafter. In the only preeclamptic patient studied, cyclic AMP was elevated in the 16-27th weeks although no clinical symptom was found until the 31st week. The study showed that the plasma cyclic AMP level in normal pregnancy becomes elevated above nonpregnant level at the end of the first and during the third trimesters. However, this profile appeared to be altered in pregnancies complicated by hypertension.
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PMID:Adenosine-3',5'-monophosphate in the plasma from human pregnancy. 19 Feb 60

The concentration of plasma adenosine 3',5'-cyclic monophosphate (cyclic AMP) and plasma renin activity (PRA) were measured concomitantly in blood from both renal veins and in arterial blood in 22 hypertensive patients. In the nine patients with true renovascular hypertension the concentration of plasma cyclic AMP was greater in the venous effluent of the kidney affected by the renal artery stenosis than in that of the unaffected or less affected kidney. The arteriovenous difference in cyclic AMP concentration was less on the affected side in all but one patient. The arteriovenous differences in PRA identified the affected kidney as the source of hyper-reninemia and showed that renin release from the other kidney was suppressed. In the 13 patients with hypertension associated with but unrelated to renal artery stenosis there were no consistent patterns of cyclic AMP concentration or PRA in the venous effluent of the kidneys or of their arteriovenous differences. In renovascular hypertension the venous effluent of the kidney affected by renal artery stenosis contains not only more renin but also more cyclic AMP, owing to either increased cyclic AMP production or decreased excretion or extraction of cyclic AMP by the affected kidney. This unilateral increase in cyclic AMP concentration may become a complementary diagnostic feature of true renovascular hypertension.
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PMID:Renal vein plasma adenosine 3',5'-cyclic monophosphate in renovascular hypertension. 19 29

In two fractions obtained from the bovine A. coronaria adenylate cyclase activity was identified and characterized. The adenylate cyclase activity of the 75,000 X g sediment shows a pH optimum at 7.4. The temperature dependence of this adenylate cyclase activity is linear when represented in the Arrhenius plot, and an Arrhenius activation energy of 13.2 kcal Mol-1 can be calculated for the enzyme reaction. The Km-value of the enzyme to ATP is 6 +/- 0.6 - 10(-4) M. The adenylate cyclase activity of the 75,000 X g sediment can be stimulated by NaF. 5'AMP and adenosine inhibit the adenylate cyclase activity of the 75,000 X g sediment. With regard to the enzyme activity, Mn++ and Co++ replace Mg++, but not Ca++. The monovalentcations Na+ and K+ do not influence the adenylate cyclase activity. In a particulate fraction containing plasma membranes, adenylate cyclase activity was also identified. This adenylate cyclase activity can be stimulated by catecholamines, noradrenaline, and isoproterenol. This stimulation can, however, only be proved for the enzyme in the coronaries of 9-week-old and 2-year-old animals. The adenylate cyclase activity from the coronaries of adult animals is not affected by catecholamines. These findings are discussed with regard to hypertension frequently found in adult animals.
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PMID:[Proof of adenylate cyclase activity in the coronary artery of cattle]. 19 28

Plasma and 24-h urinary adenosine 3':5'-monophosphate (cyclic AMP) and guanosine 3':5'-monophosphate (cyclic GMP) were measured by radioimmunoassay in 12 normal subjects, 33 patients with six types of non-neoplastic disease (cholelithiasis, peptic ulcer, coronary heart disease, hypertension, regional ileitis, and cirrhosis), and 34 patients with five types of disseminated neoplastic disease (acute myelocytic leukemia; Hodgkin's disease; and metastatic cancer of the lung, colon, and breast). In patients with non-neoplastic disease, cyclic nucleotide values in plasma and urine did not differ significantly (P greater than 0.05) from those in normal subjects. In patients with disseminated cancer, cyclic AMP values in plasma and urine likewise did not differ significantly from those in normal subjects. Plasma cyclic GMP, in contrast, was significantly elevated in all five types of cancer patients, and urinary cyclic GMP was significantly elevated (five times the normal mean) in patients with acute myelogenous leukemia and Hodgkin's disease.
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PMID:Plasma and urine cyclic guanosine 3':5'-monophosphate in disseminated cancer. 22 52

1. Seven latent hypertensive patients and seven matched controls were subjected to standardized mental stress and orthostatic provocation. 2. Mental stress increased blood pressure by approximately 25%, heart rate by 25 beats/min, plasma glycerol by 50% and plasma cyclic AMP by 25% in both groups. Plasma glucose and renin activity were unchanged. Plasma noradrenaline and adrenaline were essentially unchanged during stress. 3. There was an insignificant tendency towards higher noradrenaline levels in latent hypertensive subjects and two of these subjects displayed an exaggerated noradrenaline response to standing. 4. Our results indicate that the physiological responses to mental stress are caused by selective neuronal activation, rather than by generalized sympatho-adrenal activation. Latent hypertension does not seem to be associated with adrenergic hyperactivity or receptor supersensitivity, except possibly in individual cases.
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PMID:Sympatho-adrenal and cardiovascular response to mental stress and orthostatic provocation in latent hypertension. 23 22


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