Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of adenosine-induced hypotension on central as well as myocardial hemodynamics and metabolism were studied in five neurolept-anesthetized patients without known heart or lung diseases, who were undergoing cerebral aneurysm surgery. Adenosine (217 +/- 32 micrograms.kg-1.min-1) decreased mean arterial pressure 30% from 77 +/- 5 to 54 +/- 3 mm Hg. Cardiac filling pressures and heart rate remained unchanged during hypotension. Adenosine decreased systemic vascular resistance 50 +/- 5% while cardiac index increased 39 +/- 10%. Coronary sinus blood flow increased by 73 +/- 13% from 128 +/- 18 to 224 +/- 36 ml/min with a concomitant decrease in calculated coronary vascular resistance (66 +/- 4%). Both systemic and myocardial arteriovenous oxygen content differences decreased, and myocardial oxygen consumption decreased 42 +/- 9%. There were no alterations in myocardial fractional lactate extraction. Arterial plasma renin activity and arterial catecholamine levels were unaffected by hypotension. It is concluded that adenosine hypotension in this group of patients produced a hyperkinetic circulation in the systemic as well as in the myocardial vascular bed. Cardiac output and coronary sinus blood flow increased at the same time as myocardial oxygen consumption decreased.
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PMID:Effects of adenosine-induced hypotension on myocardial hemodynamics and metabolism during cerebral aneurysm surgery. 327 50

Adenosine may be a physiological modulator of vascular smooth muscle tone, sympathetic neurotransmission, renin release, and renal and cardiac function. To facilitate the elucidation of the physiological role of adenosine, a microassay for adenosine was developed that allows accurate quantitation of adenosine in 75 microliters of rat plasma, thus permitting multiple determinations of plasma adenosine levels in an individual rat without inducing hemodynamic perturbations due to blood loss. The technique employs a simple and rapid extraction of plasma with a reverse-phase Sep-Pak cartridge and exploits the increased mass sensitivity of microbore high performance liquid chromatography. The assay was verified by demonstrating a linear relationship between the amount of adenosine added to plasma and the amount detected by the assay, a linear relationship between the rate of adenosine infusion into rats and plasma adenosine levels, and the absence of measurable adenosine levels in plasma incubated with adenosine deaminase. The mean arterial plasma level of adenosine in the anesthetized rat was determined to be 119 +/- 28 (SD) ng/ml (n = 10). With the use of this assay, renal venous plasma levels of adenosine were found to be elevated sixfold in two-kidney, one clip Goldblatt hypertensive rats (1 week postclipping) compared with sham-operated controls. Given the known effects of adenosine on renin release, these data support a role for endogenous adenosine as a regulator of renin release in renovascular hypertension.
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PMID:Development and application of a simple microassay for adenosine in rat plasma. 330 66

The present study was undertaken to investigate the effect of adenosine on the microvasculature of the hamster kidney and the possibility of angiotensin II mediation. Renal tissue from neonatal hamsters was grafted into the cheek pouch of 33 adult hamsters. Seven to twelve days later the renal microcirculation was studied. Adenosine was tested on the pre- and postglomerular arterioles as well as on cheek pouch arterioles before and after applying an AII antagonist, saralasin. Adenosine dilated the cheek pouch arterioles and constricted the preglomerular arterioles in a dose-dependent manner. Adenosine had no effect on postglomerular arterioles. The renal vasoconstriction persisted as long as adenosine was present. Theophylline reduced the adenosine-mediated vasoconstriction of the afferent arteriole in a dose-dependent manner. These changes were not altered in the presence of saralasin at various doses, one of which was 20-fold greater than that required to abolish the vasoconstrictor response of a test dose of angiotensin II. This study indicates that the adenosine-mediated vasoconstriction of the preglomerular microvessels is not mediated via the renin-angiotensin system but may be a direct effect of adenosine.
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PMID:The selective response to adenosine of renal microvessels from hamster explants. 334 37

It is known that renal ischemia enhances the production of adenosine, which is further metabolized by xanthine oxidase, and that the inhibition of this metabolizing enzyme by allopurinol ameliorates the consequences of renal ischemia. This study was undertaken to define the effect of allopurinol on the renal responses to adenosine. It was found that 5 minutes of intrarenal infusion of adenosine in control dogs produced a typical biphasic response characterized by an initial vasoconstriction, decreasing renal blood flow by 46.3% +/- 6.0%, followed by vasodilation, increasing renal blood flow by 8.5% +/- 3.6% above the control levels. Adenosine infusion was also accompanied by a significant reduction of plasma renin activity, from 8.4 +/- 0.6 ng/ml/hour to 3.8 +/- 0.4 ng/ml/hour. The administration of an intravenous infusion of 50 mg allopurinol did not alter the vasoconstrictor phase of adenosine--the average decrease was 41.1% +/- 3.3%; however, it prevented much of the vasodilation because renal blood flow over the 5 minutes remained 17.9% +/- 5.0% less than the levels recorded before adenosine infusion. Allopurinol also prevented the decrease of plasma renin activity, for which the average values recorded before and after adenosine were 9.6 +/- 0.6 ng/ml/hour and 8.2 +/- 0.6 ng/ml/hour, respectively. The results of this study indicate that allopurinol exerts specific effects on the vasodilatory component of adenosine and prevents the adenosine-suppressive effect on the renin-angiotensin system.
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PMID:Effect of allopurinol on the renovascular responses to adenosine. 351 11

In previous studies we identified an afferent renal nerve-dependent pressor reflex elicited by acute unilateral renal artery stenosis (50% decrease in renal blood flow) in conscious, instrumented rats with reduced responsiveness of arterial baroreceptor reflexes and the renin-angiotensin system. The pressor reflex involves a neurogenic increase in peripheral resistance. The present study examined the nature of the intrarenal stimulus underlying this renal pressor reflex. Rats were subjected to sinoaortic denervation and, 7 to 10 days later, were chronically instrumented with Doppler flow probes on the right renal artery, superior mesenteric artery, and abdominal aorta and with an occluder on the right renal artery. Following surgical recovery and inhibition of the renin-angiotensin system (captopril), animals received intravenous isotonic saline, 6% of body weight over 60 minutes. Saline infusion did not alter baseline hemodynamics, vascular neurogenic tone, or responsiveness to tyramine, but it attenuated the reflex by 70%. A second series of experiments examined a possible role for intrarenal prostaglandins, kinins, or adenosine in the activation of renal sensory receptors during renal stenosis. Prostaglandin inhibition with intravenous administration of indomethacin and meclofenamate virtually abolished the reflex in the face of enhanced tyramine responsiveness, whereas kallikrein inhibition (aprotinin) attenuated the reflex pressor response by 33%. Adenosine inhibition with aminophylline or adenosine deaminase had no effect on the reflex; these agents and aprotinin did not affect vascular neuroeffector responsiveness (tyramine). The data suggest that the renal pressor reflex may be mediated by renal sensory nerves, possibly chemoreceptors, whose activation could depend on renal excretory function and synthesis of prostaglandins and kinins.
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PMID:Role of prostaglandins and kinins in the renal pressor reflex. 366 64

Adenosine produced by the macula densa cells in response to changes in the tubular NaCl-concentration has been suggested to inhibit renin release in vivo. In order to test this suggestion we studied: incubated kidney cortical slices (KS) which contain both the macula densa and the entire afferent arteriole; superfused single microdissected glomeruli (LAG) without macula densa but with the afferent arteriole preserved; and superfused batches of selected glomeruli (SAG) containing only the juxtaglomerular cells closest to the glomerulus. For superfusion and incubation a bicarbonate Ringer solution was used. The specificity of the renin release process was validated by measuring adenylate kinase as a marker for cytoplasmatic leak. Adenosine (10 micrograms/ml) halved basal renin release from incubated KS as compared to controls (P less than 0.001, n = 8, 8). Renin release from LAG stimulated by calcium depletion was also inhibited (P less than 0.05, n = 8, 9) whereas basal release was not affected (n = 6, 12). No effect was detected neither on basal nor on calcium stimulated renin release from SAG. We conclude that adenosine inhibits renin release in vitro by a mechanism independent of a functioning nephron, and which involves only the JG-cells located in the afferent arteriole at some distance from the glomerulus.
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PMID:Effects of adenosine on renin release from isolated rat glomeruli and kidney slices. 389 16

The action of theophylline on the adenosine-induced decrease in renin release was studied in anesthetized dogs. Adenosine inhibited renin release, decreased GFR and fractional sodium excretion, and decreased the concentration of angiotensin II in the renal lymph. Theophylline (5 mumol/min intrarenally) had no significant effect on GFR or RBF yet produced a significant increase in the release of renin and the fractional excretion of sodium. The intrarenal infusion of adenosine (3 X 10(-7) mol/min) during theophylline infusion produced no effect on GFR or RBF, but fractional sodium excretion and renin release were significantly decreased. Adenosine was infused at a lower dose (3 X 10(-8) mol/min) during theophylline (5 X 10(-6) mol/min) infusion in a second group of dogs. With the exception of fractional sodium excretion, all effects of adenosine were effectively antagonized by theophylline. Theophylline at 5 X 10(-6) mol/min, which stimulates renin release and effectively antagonizes the renal effects of adenosine, had no detectable effect on cAMP measured in renal cortex. Furthermore, no change in cortical cAMP was observed until theophylline was increased 50-fold over the dose effective in antagonizing adenosine. These findings demonstrate that theophylline, at concentrations having no effect on cortical cAMP, antagonizes the effect of adenosine on renin release. The results are also consistent with the view that theophylline stimulates renin release by a mechanism other than its action on cAMP.
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PMID:Antagonistic effect of theophylline on the adenosine-induced decreased in renin release. 608 79

Adenosine has been reported to produce a biphasic renal blood flow (RBF) response (vasoconstriction followed by a return of flow to control level) and a decrease in glomerular filtration rate (GFR) when infused into the kidney. Intrarenal adenosine infusion also leads to a decrease in renin release. By altering the hemodynamic response to adenosine, we sought to determine whether the decrease in renin release depends on vascular or filtration-induced events. In nine dogs with nonfiltering kidneys, adenosine infusion (3 X 10(-7) mol/min) resulted in a biphasic RBF response and an inhibition of renin release (309 +/- 53 vs. 71 +/- 26 ng ANG I/min). In 11 dogs treated with verapamil (10 micrograms X kg-1 X min-1) no vasoconstriction or decrease in GFR occurred; however, renin release was inhibited by adenosine (1,300 +/- 159 vs. 534 +/- 225 ng ANG I/min). In a third group of nine dogs whose ureteral pressure was raised to 80 cmH2O, adenosine infusion produced a sustained vasoconstriction and an inhibition of renin release (3,086 +/- 1,144 vs. 328 +/- 130 ng ANG I/min). These experiments, in which the renin release effects of adenosine are dissociated from the hemodynamic effects, lead us to conclude that the inhibition of renin release produced by adenosine does not depend either on the vascular or filtration-induced effects of adenosine.
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PMID:Adenosine-induced decrease in renin release: dissociation from hemodynamic effects. 638 77

Uridine, uridine monophosphate (UMP) and uridine diphosphate (UDP) increased blood pressure when infused into intact anaesthetized rats and had similar effects on the perfusion pressure in the rat isolated perfused kidney. In an isolated vascular preparation, the everted rat portal vein, uridine was without effect while UMP and UDP caused log dose-related increases in contractile work. Adenosine infused at a dose of 200 nmol/kg per min blocked the response to uridine in the intact rat, converting it to a depressor response at higher doses, and reduced the response to UMP. Uridine may need to be phosphorylated to UMP to act on blood vessels. The two compounds are effective at similar dose ranges and suppress renin secretion in the isolated kidney, while UDP, which is effective at lower doses and stimulates renin secretion, may act by a different mechanism. Adenosine competes for membrane transport with uridine but its inhibition of the effects of UMP is consistent with activity at intracellular sites as well.
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PMID:Vasoconstrictor effects of uridine and its nucleotides and their inhibition by adenosine. 651 66

Central and splanchnic hemodynamic effects during controlled hypotension induced by the administration of the endogenous vasodilator adenosine were studied in ten artificially ventilated dogs under neurolept anesthesia. Adenosine was administered as a continuous infusion in the aorta (n = 3), in the inferior vena cava (n = 3), and after pretreatment with dipyridamole (which inhibits the cellular uptake of adenosine) (n = 4) in a dose sufficient to maintain a mean arterial blood pressure (MABP) level of approximately 50 mmHg. Observations were made before and after 20 min of controlled hypotension. Basal arterial plasma levels of adenosine were in the 10(-7) M range (means = 0.4 microM). The hemodynamic response was similar in all three settings. Adenosine caused a profound decrease in systemic vascular resistance (SVR) (52%, P less than 0.01) and preportal vascular resistance (PPR) (64%, P less than 0.01), while hepatic arterial vascular resistance ( HAR ) increased by 49% (P less than 0.05). Cardiac output increased (22%, P less than 0.05) through increase of stroke volume (77%, P less than 0.01), while heart rate decreased (28%, P less than 0.01). Whole-body oxygen uptake decreased (14%, P less than 0.01). Portal venous blood flow increased by 28% (P less than 0.05), whereas hepatic arterial blood flow decreased by 70% (P less than 0.01). In the preportal tissues, oxygen uptake decreased by 21% (P less than 0.01). In contrast, hepatic oxygen consumption increased (53%, P less than 0.05). Adenosine-induced hypotension was not associated with changes in plasma renin activity or the plasma concentration of norepinephrine. It is concluded that adenosine causes a rapidly induced and easily maintained hypotension and may be a potentially useful agent for controlled hypotension in patients.
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PMID:Central and splanchnic hemodynamics in the dog during controlled hypotension with adenosine. 673 9


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