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

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

Prostaglandins are highly potent derivatives of unsaturated fatty acids with multiple biological activities. They are synthesized and metabolized in almost all tissues studied so far. The E- und F-type prostaglandins may be regarded as local modulators of hormonal effects on cell function and--in some cases (kidney, uterus-corpus luteum)--as regional or tissue hormones. Thus they seem to be involved in the regulation of neurotransmission, kidney function, triglyceride metabolism in adipose tissue and progesterone biosynthesis. Apart from their influence on renal blood flow prostaglandins of the A-type possibly have an additional function as circulatory hormones regulating blood pressure. Second messenger-systems (cAMP, Ca++-cGMP) which mediate the effects of most non-steroidal hormones are also involved in the action of prostaglandins, at least of the E-and F-types. Disturbances in prostaglandin metabolism (increased or decreased biosynthesis) are discussed to play a role in the pathogenesis of inflammation, pain, fever, hypertension, bronchial asthma and gastric or duodenal ulcer formation. Drugs with antiinflammatory, analgesic and antipyretic activity have been shown to be potent inhibitors of prostaglandin formation. The correlation of a local prostaglandin deficit or the therapeutic use of single effects of prostaglandins by administration of exogenous compounds (natural prostaglandins or modified derivatives) has so long been less satisfactory because of their large number of biological actions which lead to undesired side effects. Extensive experience have been obtained in the successful induction of therapeutic abortion. This effect is based on the stimulatory action of E- and F-type prostaglandins on the smooth muscles of the pregnant uterus which is resistent to the influence of other stimuli, e. g. oxytocin. Here the incidence of side effects could be reduced by local administration of low doses of prostaglandins into the uterine cavity. A general improvement of the therapeutic usefulness of prostaglandins will however only be achieved, if modified derivatives with more specific actions on the desired "target" tissues are available.
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PMID:[Biology of prostaglandins with reference to therapeutic aspects]. 16

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

In order to test the hypothesis that the activity of cardiovascular centres is determined by their content of cAMP a number of drugs which influence the activity of either phosphodiestase or adenylcyclase were injected in doses of 100-1000 mug/kg into the lateral cerebral ventricle of cats. The effects on blood pressure and heart rate were studied. The phosphodiesterase inhibitors papaverine, carbocromene, theophylline and caffeine caused hypertension and tachycardia which increased with the dose while the phosphodiesterase activator imidazole exerted opposite effects. Sodium fluoride which activates adenylcyclase increased blood pressure and heart rate substantially. The results confirm the above-mentioned hypothesis.
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PMID:Further evidence for the involvement of cAMP in central blood pressure regulation. 18 30

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

In the course of investigations on experimental arterial hypertension in rats, it has been stated, that imipramine prevents the development of hypertension and that is simultaneously causes an accumulation of cAMP in the vessel walls. The relationship between the two phenomena has been discussed.
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PMID:The role of cyclic adenosine 3',5'-monophosphate (cAMP) in the mechanism of action of tricyclic antiderpressants. 19 49

The authors examined the concentration of cAMP in the myocardium of rats with experimental hypertension during various periods after modeling of the process. The changes in the values of cyclic nucleotide corresponded to the dynamics of the development of the arterial hypertension. There was na increase of the level of cAMP in the myocardium on the third day after modeling of hypertension, accompanying the initial elevation of the arterial pressure. The maximal values of cAMP were established on the 30th day, which corresponded to the maximal development of hypertension. Cyclic 3,5-adenomonophosphate began to diminish parallel to the lowering of the arterial pressure during the chronic phase 90th day. The obtained results give a possibility to discuss the participation of cAMP in the pathogenesis of myocardial hypertension, occurring in experimental hypertension.
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PMID:[Participation of cyclic-3',5'-adenosine monophosphate in the pathogenesis of myocardial hypertrophy in experimental hypertension]. 20 46

The content of cyclic nucleotides (cAMP and cGMP) in the blood plasma, urine and tissues, and also morphological changes of the vascular renal bed were studied in rats with arterial hypertension induced by chronic inhibition of prostaglandin synthesis. A considerable thickening of the wall of the interlobular and arcuate arteries with marked lumen narrowing occurred mainly on account of hypertrophy and the swelling of smooth muscle cells. At the same time there was a marked increase in the cGMP concentration, a decrease of cAMP level, and a reduction of the cAMP/cGMP coefficient in the biological fluids. It is suggested that the changed cyclic nucleotides metabolism is associated with organic and functional changes of the peripheral vascular bed underlying an increase of the total vascular resistance in arterial hypertension.
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PMID:[Several pathogenetic factors of experimental "indomethacin" hypertension]. 21 Aug 60

As compared to fatty tissue cells of animals with normal pressure, those of SHR rats were found to be characterized by a higher lipolytic response and a larger increase in the cAMP content on exposure to the effect of ACTH. As compared to the controls, adrenalectomized SHR rats had an increased basal cAMP content and an increased lipolytic response of the adipocytes following adrenaline administration. In inhibition of phosphodiesterase in the fatty cells of adrenalectomized rats with normal pressure, the cAMP content grew by 20% as compared to that in SHR rats subjected to the operation. It is suggested that the changes in intracellular distribution of calcium, shown in this model of hypertension, may be the direct cause of the altered sensitivity of the "target" cells to the effect of hormones.
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PMID:[Mechanism of the change in adipocyte sensitivity to ACTH and adrenaline in spontaneous genetic hypertesion in rats]. 21 34

The reaction of cyclic nucleotides in blood to an orthostatic position, furosemid administration, and submaximal bicycle ergometry load was studied in 20 healthy individuals and in 50 patients with hypertensive disease. A special group was composed of 25 patients the disease in whom was marked by crises. It is shown that a walk of one hour and intravenous infusion of 40 mg of furosemid caused an increase in the blood cAMP but did not change the level of cGMP. During a bicycle ergometry load the levels of cGMP and cGMP increased to an equal measure and returned to their initial values 30 min after its cessation. In patients with arterial hypertension the cGMP system becomes most functionally mobile, whereas the cAMP level, if it increases, does so at a later term after the effect of the stimulus begins. The increased cGMP level is maintained for quite a lengthy period of time after the load is discontinued. In patients suffering from hypertensive disease with crises the cAMP/cGMP ratio, which is reduced at rest also, diminishes still more in an orthostatic position and particularly during a crisis. The role of changes in the metabolism of cyclic nucleotides and their sensitivity to regulatory factors in the pathogenesis of arterial hypertension is discussed.
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PMID:[Cyclic nucleotides in the blood plasma in arterial hypertension]. 21 19


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