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)

Acute caffeine in subjects who do not normally ingest methylxanthines leads to increases in blood pressure, heart rate, plasma epinephrine, plasma norepinephrine, plasma renin activity, and urinary catecholamines. Using a double-blind design, the effects of chronic caffeine administration on these same variables were assessed. Near complete tolerance, in terms of both humoral and hemodynamic variables, developed over the first 1-4 d of caffeine. No long-term effects of caffeine on blood pressure, heart rate, plasma renin activity, plasma catecholamines, or urinary catecholamines could be demonstrated. Discontinuation of caffeine ingestion after 7 d of administration did not result in a detectable withdrawal phenomenon relating to any of the variables assessed.
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PMID:Tolerance to the humoral and hemodynamic effects of caffeine in man. 700 53

The effects of caffeine and ethanol on treadmill performance and metabolic responses to exercise were determined in four trained runners. Caffeine (2.5 mg.kg-1 body weight) or ethanol (25 ml) in 150 ml of grapefruit juice (total volume) or grapefruit juice (placebo) was randomly administered 10 minutes prior to and at 30 minutes of a 60 minutes treadmill run. The speed and grade of the treadmill was adjusted to elicit an average oxygen consumption of 80-85% of the subject's maximal oxygen consumption. All subjects completed the treadmill run for the caffeine and placebo conditions. Three of the four subjects could not complete the treadmill run following the second administration of ethanol. Exercise heart rate was significantly greater for the ethanol condition than for the placebo condition. Exercise oxygen consumption was greater following ethanol administration than for placebo, but the differences were not significant. Blood glucose rose significantly between 0 and 30 minutes of treadmill running for all three conditions. Between 30 minutes of treadmill running and either 60 minutes or the time of termination of the exercise, blood glucose decreased significantly by 24% following the second ethanol treatment. Plasma fatty acid, triglyceride, creatine phosphokinase, and renin contents followed expected exercise changes with a blunting of the rise of plasma fatty acids at 30 minutes of exercise for the ethanol condition. It was concluded that the administration of ethanol adversely influenced treadmill exercise performance by eliciting a hypoglycemic effect between 30 minutes and the termination of the exercise.
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PMID:Effects of caffeine or ethanol on treadmill performance and metabolic responses of well-trained men. 783 61

First, this investigation showed that plasma levels of inosine, hypoxanthine, and xanthine, which are metabolites of adenosine, rose sharply when blood pressure dropped suddenly along with symptoms during a hemodialysis session (sudden hypotension), but not when it decreased gradually with eventual symptoms (gradual hypotension). Because adenosine has an action to dilate vessels, this result indicates the possibility that the increased release of adenosine would be a cause of sudden hypotension. Second, it was found that the frequency of sudden hypotension decreases with the administration of caffeine, which is an adenosine-receptor antagonist, whereas the frequency of gradual hypotension did not change. This result supports the above-mentioned hypothesis that adenosine may well be a mediator of sudden hypotension, but not of gradual hypotension. Third, our investigation demonstrated no significant differences in plasma norepinephrine level, in plasma renin activity, or in mean blood pressure between the hemodialysis session in which caffeine was administered and the session in which a placebo was given. These findings suggest that the effect of caffeine administration to prevent sudden hypotension is not mediated by the stimulation of the sympathetic nervous system or activation of the renin-angiotensin system, but by the adenosine-receptor antagonism.
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PMID:Role of adenosine in dialysis-induced hypotension. 791 52

In the present study we used radiotelemetry technology to investigate: 1) the time course for development of hypertension in 2-kidney, 1-clip (2K1C) rats and 2) the effect of chronic caffeine consumption on blood pressure in 2K1C rats. Rats received water or caffeine (0.1%) in drinking water and were instrumented with radiotelemetry devices to permit continuous monitoring of blood pressure. A clip was placed on the left renal artery of rats in both the water (WATER/CLIP) and caffeine (CAFFEINE/CLIP) groups. The clip was applied briefly to, then removed from, the renal artery of caffeine- and water-treated rats randomized to the sham-operated (SHAM) group. Mean arterial blood pressure (MABP) increased by approximately 35 mm Hg within 2 hr of clipping. MABP in the WATER/CLIP and CAFFEINE/CLIP groups differed significantly from the SHAM group, but not from each other, for the first 10 days after clipping. Thereafter, MABP was greater in the CAFFEINE/CLIP rats as compared to WATER/CLIP rats. At 4.5 weeks after clipping, MABP values differed significantly in the CAFFEINE/CLIP, WATER/CLIP and SHAM rats (140 +/- 4, 122 +/- 4 and 103 +/- 2 mm Hg, respectively). Involvement of the renin-angiotensin system was assessed by treatment with the AT1 receptor antagonist, losartan, and the converting enzyme inhibitor, captopril. Results from this study indicate: 1) hypertension develops rapidly after clipping in rats monitored with telemetry; 2) the renin-angiotensin system is involved in maintaining hypertension in 2K1C rats even beyond 4 weeks after clipping; and 3) caffeine augments the increase of blood pressure in 2K1C rats, apparently through the involvement of the renin-angiotensin system.
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PMID:Telemetric blood pressure monitoring in benign 2-kidney, 1-clip renovascular hypertension: effect of chronic caffeine ingestion. 793 54

We explored the hypothesis that chronic blockage of adenosine (Ado) receptors might augment the renin response to sodium restriction. In addition, an ancillary topic has been undertaken to test the hypothesis that endogenous Ado would restrain plasma norepinephrine (NE) and epinephrine (E) release. Male Sprague-Dawley rats (250 +/- 20 g) were fed with low sodium chow (Na+ 0.03%) and drank either distilled water or caffeine containing water (0.1%). Blood pressures were recorded in the presence of different concentrations of Ado. Plasma renin activity was measured at the beginning, 1 week and 6 weeks after the low sodium diet. An in situ autoperfused rat kidney model was used to examine whether renal function was influenced by chronic inhibition of Ado receptors. Furthermore, the effect of theophylline on cardiovascular actions of Ado in anaesthetized rats, and the effect of 1,3-dipropyl-8-(p-sulfophenyl)xanthine (DPSPX) on acute hydralazine induced NE and E release in conscious, unrestrained rats were also determined. Our data showed that the inhibitory effect of Ado on renin activity and blood pressure in salt restricted rats was attenuated by caffeine at the first week but not at six weeks after institution of the low sodium diet. Renal function in sodium restricted rats did not change after chronic caffeine consumption. Theophylline attenuated the dose-related inhibitory actions of Ado on blood pressure. Finally, DPSPX significantly increased plasma catecholamines, and these effects were much greater in rats treated with hydralazine. We conclude that the augmented renin response is not continued during chronic blockage of Ado receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of adenosine blockade on plasma renin activity and catecholamines. 823 40

Non-modulation has been proposed as an intermediate phenotype in human essential hypertension. The trait is characterized by blunted aldosterone and renal plasma flow responses to short-term angiotensin II (Ang II) infusion. Elevated tissue Ang II levels or decreased tissue adenosine levels could account for this decreased sensitivity to Ang II. In support of the latter possibility, endogenous adenosine has been shown to contribute to the renal vasoconstrictive response to Ang II in animals. We therefore tested the hypothesis that endogenous adenosine contributes to modulation of renal plasma flow in sodium-replete humans. We examined the effect of long-term administration of the adenosine receptor antagonist caffeine on baseline renal plasma flow and on the renal plasma flow response to short-term Ang II infusion in six salt-replete normotensive subjects in a single-blind, placebo-controlled study. para-Aminohippurate clearance was used to assess renal plasma flow. Ang II was infused in graded doses (0.3 to 3 ng/kg per minute) in the presence and absence of caffeine (250 mg PO TID for 7 days). Blood pressure, plasma renin activity, Ang II, electrolytes, and para-aminohippurate clearance were measured before and after each dose of Ang II. Caffeine did not alter either baseline blood pressure or the blood pressure response to Ang II but did increase baseline plasma renin activity from 0.72 +/- 0.09 to 1.42 +/- 0.26 ng angiotensin I/mL per hour (P = .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Caffeine attenuates the renal vascular response to angiotensin II infusion. 824 16

The present study was aimed to determine the effect of caffeine on the development of renal hypertension. Two-kidney, 1-clip (2K1C) hypertension and deoxycorticosterone acetate (DOCA, 200 mg/kg, subcutaneous implantation)-salt (0.9% NaCl drinking) hypertension were instituted in Sprague-Dawley rats. They were then grouped into two groups each: one was supplemented with caffeine (0.1%) in their drinking solution and the other was not. Systolic blood pressure was measured up to 24 days. Caffeine exacerbated the development of 2K1C hypertension in association with a higher plasma renin concentration (PRC). Caffeine ingestion, however, did not exacerbate but ameliorated DOCA-salt hypertension in which PRC was comparable between the caffeine-ingested and control groups. Concentrations of plasma atrial natriuretic peptide (pANP) were significantly different between the caffeine-ingested and control groups neither in 2K1C nor in DOCA-salt rats, suggesting that ANP was not responsible for the modified blood pressure. Acute caffeine infusion (350 micrograms/min, 30 min) in anesthetized normotensive rats caused increases in urinary excretion (volume and sodium) and in PRC without significantly affecting the blood pressure and pANP. These results suggest that caffeine specifically exacerbates 2K1C hypertension through increasing renin release whereas it ameliorates DOCA-salt hypertension possibly through increasing renal excretion.
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PMID:Chronic caffeine ingestion exacerbates 2-kidney, 1-clip hypertension and ameliorates deoxycorticosterone acetate-salt hypertension in rats. 830 20

In young hypertensive patients, after a short period of abstention, caffeine ingestion has a significant pressor effect, although the acute cardiovascular responses have not been reported in elderly hypertensives. This study assessed the acute changes in BP, pulse rate, plasma renin activity (PRA) and arterialised plasma catecholamines after 250 mg of caffeine and matching placebo following 12 and 48 hours of caffeine abstention. After 48 hours caffeine abstention supine SBP was higher over the 120 minute study period following acute caffeine loading than following placebo (10 mmHg; 95% Cl 3-17 mmHg, P = 0.016) although the overall post-caffeine rise from baseline values was small (2 mmHg; -3 to 8 mmHg, P = 0.30). Similar differences were seen for supine DBP and standing SBP and DBP although pulse rate was unchanged throughout. After 12 hours abstention no acute pressor effect of caffeine was seen, in fact SBP fell over the study period (-5 mmHg; -10 to 0 mmHg, P = 0.05), and there was no difference between the caffeine and placebo phases. No change in plasma catecholamines or PRA values was found during any of the phases. These results suggest that in elderly hypertensives the pressor effect of caffeine (the equivalent of two to three cups of coffee) is small even after prolonged abstention. After the shorter abstention period, of the duration likely to be seen in clinical practice, no pressor response to caffeine was demonstrated. It is unlikely that acute caffeine ingestion has a significant effect on clinic BP measurements in elderly hypertensives who are regular caffeine consumers.
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PMID:Blood pressure, plasma catecholamine and renin responses to caffeine in elderly hypertensives. 834 95

Animals treated acutely with an adenosine receptor antagonist have elevated plasma renin activity. This observation suggests that endogenous adenosine plays a physiologically significant role in restraining renin release. However, it is unclear whether chronic blockade of adenosine receptors would cause a rise of renin activity since tolerance to adenosine blockade is known to develop quickly. An earlier study partially addressed this question by showing that chronic blockade of adenosine receptors with caffeine exacerbated both the rise of plasma renin activity and the decline of renal function in 2-kidney-1-clip (2K1C) renovascular hypertensive rats. However, that study did not determine whether the difference in renin activity occurred solely as a secondary result of the difference in renal function. The purpose of this study was to reexamine the effect of chronic caffeine consumption on plasma renin activity and angiotensin I levels in animals in another high-renin model, i.e., the low sodium diet. The low sodium diet is devoid of the potential confounding effect of deteriorating renal function associated with the 2K1C renovascular hypertension model. In this study, animals received normal rat chow and drank either 0.1% caffeine water or vehicle for ten days. After ten days, all rats were switched to a low sodium diet for three weeks. Plasma renin activity and plasma angiotensin I levels were measured before, and at 1 and 3 weeks after initiating the low sodium diet. The results of this study show that chronic blockade of adenosine receptors with 0.1% caffeine water increases plasma renin activity and angiotensin I concentration before and throughout the three weeks when animals were on the low sodium diet. The results of this study suggest that the inhibitory role of adenosine on renin release is a general physiological process, rather than a special situation applicable only to the 2K1C model.
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PMID:Effect of caffeine treatment on plasma renin activity and angiotensin I concentrations in rats on a low sodium diet. 844 83

Effects of caffeine on ambulatory blood pressure, heart rate, renin-angiotensin system, and ANP were studied in patients treated for mild to moderate hypertension in a randomized, double-blind, placebo-controlled, cross-over trial comparing 2 weeks of caffeine-free diet with 2 weeks of regular coffee use. Twenty-three patients (13 men; aged 28-74 years) with treated, mild to moderate essential hypertension and a regular intake of 3-4 cups of coffee daily completed the study. Mean 24-h, day- or night-time ambulatory blood pressure and heart rate were not different between regimens. Nor were there any effects on the renin-angiotensin system while ANP was significantly increased during caffeine intake. Compliance of the dietary regimen was excellent as assessed by serum caffeine concentration measurements. We conclude that habitual coffee drinking did not influence the 24-h blood pressure profiles or cardiovascular hormones in treated hypertensives.
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PMID:Effect of coffee on ambulatory blood pressure in patients with treated hypertension. 846 68


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