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

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

Morphologic observations suggest that the inner layers of the thoracic aorta in man and dog are avascular and the outer layers have vasa vasorum. It appears that vasa vasorum are essential in the thoracic aorta because their interruption produces medial necrosis. These experiments provide the first measurements of blood flow through aortic vasa vasorum and examine physiologic regulation of that flow. During control conditions the outer two-thirds of the media of the thoracic aorta received 10 ml/min per 100 g blood flow through vasa vasorum. Flow to the inner third of the aorta was 1 ml/min per 100 g. Flow to both the inner and outer media of the abdominal aorta was less than 1 ml/min per 100 g. Adenosine increased blood flow to vasa vasorum in the outer media of the thoracic aorta from 7 to 18 ml/min per 100 g, but did not increase flow to the inner layers of the aorta. Hemorrhagic hypotension decreased flow in the outer media of the thoracic aorta from 14 to 2 ml/min per 100 g. Acute hypertension failed to increase blood flow through vasa vasorum, as conductance decreased significantly. These studies indicate that vasa vasorum provide a considerable amount of blood flow to the outer layers of the thoracic aorta. The vessels are responsive to physiologic stimuli because they dilate during infusion of adenosine and constrict during both hemorrhagic hypotension and acute hypertension. We speculate that the failure of blood flow to the aortic wall to increase during acute hypertension might, if it were sustained, contribute to aortic medial necrosis.
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PMID:Regulation of blood flow to the aortic media in dogs. 65 26

Administration of adenosine results in profound hypotension without the expected activation of reflex sympathetic and renin mechanisms in most animal models. This action can be explained by the vasodilatory and neuroinhibitory effects of adenosine. It is generally considered an inhibitory neuromodulator because it inhibits the release of virtually all neurotransmitters studied and produces hyperpolarization of neurons. In contrast, adenosine produces vasoconstriction of some vascular beds, including the renal and pulmonary circulations. Renal vasoconstriction is caused by activation of A1 receptors and involves an interaction with angiotensin II. In other vascular beds adenosine releases eicosanoids, including thromboxane, also resulting in vasoconstriction. Adenosine-induced vasoconstriction is transient and species dependent. Neither the receptor type, the molecular mechanisms of these actions, nor their significance to pathophysiological processes have been defined. Adenosine also has an apparent excitatory effect in the nucleus tractus solitarii. Microinjections of adenosine into this brain stem nucleus lead to decreased sympathetic tone and hypotension similar to those produced by the excitatory amino acid glutamate. The mechanism that explains this action has recently been explored and involves the release of glutamate by adenosine. Adenosine also stimulates afferent fibers mediating sympathetic activity, including renal and myocardial afferent nerves, and carotid and aortic chemoreceptors. Afferent nerve activation seems to be more pronounced in humans and may explain most of the cardiovascular and respiratory actions of adenosine in this species. Finally, animal studies suggest that endogenous adenosine plays a role in the regulation of the baroreceptor reflex and restrains the full expression of renin-dependent hypertension.
Hypertension 1992 Oct
PMID:Contrasting excitatory and inhibitory effects of adenosine in blood pressure regulation. 139 81

In vitro data indicate that the activation of A2 adenosine receptors increases renin release by the accumulation of cyclic AMP. Because in human forearm vessels beta-adrenergic receptor stimulation causes the local release of renin and angiotensin II through the increase of cyclic AMP, we evaluated in six essential hypertensive subjects whether adenosine can release vascular angiotensin II. Adenosine was infused into the brachial artery at cumulatively increasing doses (0.5, 1.5, and 5 micrograms/100 ml forearm tissue per minute for 5 minutes each) during saline infusion and in the presence of the adenosine antagonist theophylline (100 micrograms/100 ml forearm tissue per minute for 15 minutes), while venous (ipsilateral deep forearm vein) and arterial (brachial artery) angiotensin II (picograms per milliliter) were measured at the end of each infusion period, and forearm angiotensin II net balance (picograms per minute) was calculated by venous-arterial differences corrected for forearm blood flow (strain-gauge venous plethysmography) and hematocrit. In control conditions, adenosine, at higher doses, caused a dose-dependent vasodilation and increased venous angiotensin II without affecting arterial values; therefore, the calculated angiotensin II net balance showed an adenosine-mediated dose-dependent release. Theophylline pretreatment blunted adenosine-mediated forearm blood flow increments and angiotensin II release. The local origin of angiotensin II was further confirmed in another group of six hypertensive subjects in whom the angiotensin converting enzyme inhibitor captopril, locally infused at the rate of 2.5 micrograms/100 ml forearm tissue per minute for 15 minutes, abolished the adenosine-mediated venous angiotensin II increments. Our data indicate that exogenous adenosine can stimulate the production of angiotensin II in the forearm vessels of hypertensive patients.
Hypertension 1992 Jun
PMID:Adenosine activates a vascular renin-angiotensin system in hypertensive subjects. 159 66

Adenosine A1 agonists have been shown to induce a variety of pharmacological effects. In New Zealand White rabbits, the topical administration of 500 micrograms of the relatively selective adenosine A1 receptor agonist R(-) phenylisopropyladenosine (R-PIA) produced a biphasic response in IOP in the ipsilateral eye: an initial ocular hypertension (3.5 +/- 1.4 mm of Hg) at 0.5 hour, followed by significant reduction in IOP (5 to 8 mm of Hg) from 2 to 6 hours postadministration. The IOP response to 50 and 165 micrograms of R-PIA demonstrated that the ocular hypotensive response to R-PIA was dose-related; however, no initial hypertension was observed at these lower doses. The ocular response to R-PIA was primarily unilateral with only a small reduction in contralateral IOP at 1 hour observed in animals treated with 500 micrograms. No significant change in pupil diameter was observed with any dose of R-PIA. Pretreatment with the adenosine antagonist CPT (10 mg/kg; i.p.) significantly inhibited the ocular hypotensive response to R-PIA. However, pretreatment with the cyclooxygenase inhibitor indomethacin (50 mg/kg; i.p.) did not alter the change in IOP induced by R-PIA. The administration of R-PIA once a day for five days demonstrated that tolerance does not develop in rabbits with repeated administration. These data demonstrate that the adenosine A1 agonist R-PIA can lower IOP. The unilateral nature and the inhibition by CPT supports the idea that this response is mediated by adenosine receptors located in the eye.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ocular hypotensive activity of the adenosine agonist (R)-phenylisopropyladenosine in rabbits. 160 41

Adenosine is an inhibitory neuromodulator in several brain regions. In the nucleus tractus solitarius (NTS), however, adenosine exerts excitatory cardiovascular effects. The purpose of the present study was to elucidate the involvement of other endogenous mechanisms that could contribute to the final hemodynamic response to adenosine in this nucleus. In normotensive Sprague-Dawley rats, intra-NTS microinjection of adenosine (2.3 nmol/60 nl) decreased blood pressure and heart rate. These effects were blocked by prior administration of the specific adenosine receptor antagonist 1,3-dipropyl-8-p-sulfophenylxanthine (0.92 nmol) and by the two glutamate receptor antagonists kynurenic acid and glutamic diethylester. The specificity of the adenosine-glutamate interaction in the NTS was demonstrated with adrenergic and angiotensin receptor antagonists that did not affect the adenosine response and by experiments with glutamate receptor antagonists that did not affect nicotine actions in the NTS. Furthermore, an increase in glutamate levels was demonstrated during perfusion of adenosine through a microdialysis probe in the NTS of anesthetized rabbits. These findings indicate that adenosine increases the release of glutamate in the NTS and, thus, are at variance with the concept of a "universal" inhibitory effect of adenosine in the central nervous system.
Hypertension 1991 Oct
PMID:Cardiovascular excitatory effects of adenosine in the nucleus of the solitary tract. 168 Aug 12

Arterial pressure, cardiac mass and coronary flow reserves were measured in untreated and chronically pindolol-treated rabbits, prepared as either one-kidney one clip (1K1C) hypertensive or uninephrectomized (sham) controls. Pindolol (200 micrograms/kg/day) was administered for either 23 or 30 days, beginning 1 week after, or the day of initial surgery, respectively. Coronary flow was measured, at day 30, using radioactive microspheres, during base-line and adenosine infusion (0.4 mg/kg/min) in anesthetized open-chest preparations. Heart weight of untreated 1K1C animals (9.13 +/- 0.73 g) was significantly greater than the controls (7.19 +/- 0.77 g). Myocardial mass of 1K1C (9.93 +/- 0.86 g) and sham controls (7.40 +/- 0.31 g) were unaffected by chronic pindolol for 23 days. Cardiac hypertrophy was prevented in 1K1C animals treated with pindolol for 30 days (7.53 +/- 1.28 g). Untreated 1K1C animals were hypertensive compared to sham controls (116 +/- 12 and 78 +/- 7 mm Hg) and neither pindolol regime affected blood pressure. Bradycardia was evident in all pindolol-treated animals. Base-line coronary flow was higher in the untreated 1K1C animals compared to untreated controls (228 +/- 43 vs. 182 +/- 31 ml/min/100 g). After chronic pindolol treatments, 1K1C base-line blood flows were reduced (158 +/- 48 and 175 +/- 59 ml/min/100 g, for 23- and 30-day protocols). Adenosine vasodilated flows were not different between the untreated 1K1C and sham animals and were not affected by pindolol treatment. Therefore, hypertension and cardiac hypertrophy were dissociable in this model when pindolol was administered from the onset of hypertension. This suggests immediate involvement of beta adrenergic activation in the development of hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of cardiac hypertrophy in renal hypertensive rabbits with pindolol. 182 40

Adenosine is known to regulate myocardial and coronary circulatory functions. Adenosine not only dilates coronary vessels, but attenuates beta-adrenergic receptor-mediated increases in myocardial contractility and depresses both sinoatrial and atrioventricular node activities. The effects of adenosine are mediated by two distinct receptors (i.e., A1 and A2 receptors). A1 adenosine receptors, located in atrial and ventricular myocardium and sinoatrial/atrioventricular nodes, are responsible for inhibition of adenylyl cyclase activity. A2 adenosine receptors, located in coronary endothelial and smooth muscle cells, are responsible for stimulation of this enzyme activity. During increased myocardial oxygen demand due to rapid pacing and exercise, although both coronary blood flow and adenosine concentrations in the myocardium and coronary efflux increased, there is no clear consensus explaining its cause and effect relation at present. However, ischemia/reperfusion-induced coronary hyperemia is believed to be mostly attributed to released adenosine, and it has been proven that adenosine attenuates the severity of ischemia due to its coronary vasodilatory action. The beneficial effects of adenosine during ischemia/reperfusion processes do not seem simple. This is because myocardial ischemia and reperfusion injury is caused by 1) activated leukocytes and platelets, 2) ATP depletion and calcium overload of myocardium, and 3) catecholamine release from the presynaptic nerves as well as 4) the impaired coronary circulation. Intriguingly adenosine attenuates all of these deleterious actions and thereby attenuates ischemia/reperfusion injury. Indeed, adenosine attenuates the severity of contractile dysfunction (myocardial stunning) and limits the infarct size. Thus, administration of adenosine or potentiators of adenosine production in the ischemic myocardium may be beneficial for the attenuation of ischemic and reperfusion injuries, although further clinical investigations are necessary.
Hypertension 1991 Nov
PMID:Adenosine, the heart, and coronary circulation. 193 58

Adenosine has been shown recently to be the main factor responsible for the trophic effects of sympathetic innervation. As sympathetic denervation causes hypertrophic and hyperplastic changes reminiscent of those occurring in blood vessels of spontaneously hypertensive rats, we decided to study the effect of a continuous blockade of adenosine receptors on both blood vessel structure and blood pressure. A continuous infusion of 1,3-dipropyl-8-sulfophenylxanthine (DPSPX; 30 micrograms/kg per h for 7 days) to Wistar rats caused hyperplastic changes in peritoneal fibroblasts and mesenteric arterioles, hypertrophic changes in the smooth muscle of the tail artery and significant increase in the size of left ventricle myocardial cell nuclei. Both diastolic and systolic blood pressure increased significantly above control values. The results confirmed the trophic effects of adenosine and showed that chronic blockade of adenosine receptors causes arterial hypertension.
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PMID:Long-term administration of 1,3-dipropyl-8-sulfophenylxanthine causes arterial hypertension. 205 Jan 86

Inhibition of cyclooxygenase enhances mesenteric vascular responses to periarterial (sympathetic) nerve stimulation (PNS) in 16-week-old spontaneously hypertensive rats (SHR), but not in 25-week-old SHR. In contrast, cyclooxygenase inhibition enhances mesenteric vascular responses to PNS similarly in 16- and 25-week-old Wistar-Kyoto normotensive rats (WKY). Thus, the modulation of noradrenergic neurotransmission by endogenous PGs becomes defective as SHR age, whereas in WKY this does not occur. The purpose of this study was to determine to what extent alterations in the concentrations of PGs and/or biological response to PGs contribute to this age/hypertension-related abnormality in SHR. All studies were conducted in the in situ autoperfused rat mesentery, and plasma levels of PGE2 and 6-keto-PGF1 alpha were determined by negative-ion, chemical-ionization, gas chromatography-mass spectrometry after derivatization and clean-up of samples by two thin-layer chromatographic steps. Base-line mesenteric venous plasma levels of PGs were similar in 16-week-old SHR vs. 16-week-old WKY; however, base-line levels of PGE2 were approximately 6-fold greater than base-line levels of 6-keto-PGF1 alpha in both strains. PNS at 7 Hz approximately doubled mesenteric venous plasma levels of PGE2 in both 16-week-old SHR and WKY, but PNS did not increase levels of 6-keto-PGF1 alpha in either strain. Inasmuch as mesenteric venous plasma levels of PGE2 were responsive to PNS, the effect of aging on PGE2 levels was studied. In both strains, the base-line mesenteric venous plasma levels of PGE2 and the PNS-induced increase in PGE2 levels were similar in 16-week vs. 25-week-old animals. In 16-week-old SHR, infusions of PGE2, arachidonic acid and PGI2 directly into the mesenteric artery inhibited vascular responses to PNS. However, in 25-week-old SHR, even high doses of PGE2 or arachidonic acid failed to inhibit vascular responses to PNS, and the inhibitory potency of PGI2 was shifted 10-fold to the right compared to 16-week-old SHR. In contrast, PGE2 and arachidonic acid had similar effects on neurotransmission in 25-week-old WKY compared to 16-week-old WKY, and aging had a lesser effect on the inhibitory potency of PGI2 (i.e., 3-fold rightward shift of the dose-response curve). Adenosine also inhibited vascular responses to PNS; however, the inhibitory potency of adenosine was only slightly and similarly affected by aging in SHR and WKY.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Defective modulation of noradrenergic neurotransmission by exogenous prostaglandins in aging spontaneously hypertensive rats. 255 20


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