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)

To investigate the role of liver nerve activity on hepatic glucose production during exercise, liver-transplant subjects (LTX, n = 7, 25-62 yr, 4-18 mo postoperative) cycled for 40 min, 20 min at 52 +/- 3% (SE) maximal O2 consumption (VO2max) and 20 min at 83 +/- 1% VO2max, respectively. Kidney-transplant (KTX) and healthy control subjects (C) matched for sex and age exercised at the same %VO2max as LTX. VO2max was lower in both LTX (1.59 +/- 0.12 l/min) and KTX (1.59 +/- 0.07) than in C (2.60 +/- 0.26). At rest plasma renin and insulin were higher and plasma adrenocorticotropic hormone and cortisol lower in transplant corticosteroid-treated subjects compared with C. In LTX, hepatic glucose production (Ra) increased from 11.9 +/- 0.9 (rest) to 17.6 +/- 1.8 and 25.5 +/- 1.8 mumol.min-1.kg-1 at 52 and 82% VO2max, respectively. Peripheral glucose uptake was similar to Ra, and glucose remained at basal postabsorptive levels. During exercise the Ra increase as well as norepinephrine, insulin, and growth hormone responses were similar in LTX compared with both KTX and C. The increase in epinephrine was smaller in LTX than in C, the only group showing an increase in cortisol. The increase in plasma renin activity during exercise was attenuated in KTX compared with LTX and C. During exercise blood lactate rose more and plasma glycerol and free fatty acid levels were lower in LTX and KTX compared with C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose homeostasis during exercise in humans with a liver or kidney transplant. 773 62

The goal of this study was to test the hypothesis that increasing or decreasing the load on baroreceptors in the right heart influenced the secretion of arginine vasopressin (AVP), adrenocorticotropic hormone (ACTH), and renin during a state of sustained arterial hypotension. The hypothesis was tested in chronically instrumented conscious dogs prepared with inflatable cuffs around the pulmonary artery (PA) and the thoracic inferior vena cava (IVC). In one protocol (n = 5), mean arterial pressure was reduced 10 or 20% below control by constriction of the PA, a maneuver that caused a fall in left atrial pressure (LAP) and an increase in right atrial pressure (RAP). Plasma AVP, ACTH, atrial natriuretic peptide (ANP), and plasma renin activity (PRA) all increased (P < 0.05) in response to constriction of the PA. Reducing RAP to control by constriction of the IVC during maintained constriction of the PA had no effect on MAP, LAP, plasma AVP, ACTH, or PRA, but plasma ANP fell significantly. In a separate protocol (n = 4), constriction of the IVC was used to reduce MAP 10 or 20% below control, and this led to significant decreases in both LAP and RAP and increases in plasma AVP, ACTH, and PRA. RAP was then increased above control by constriction of the PA without altering either MAP or LAP. Raising RAP from a level that was 6.3 +/- 1.3 mmHg below control to 3.5 +/- 1.0 mmHg above control had no effect on plasma AVP, ACTH, or PRA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of loading right atrial and ventricular receptors on stimulated AVP, ACTH, and renin secretion in awake dogs. 773 89

Our followup study of 48 patients with primary aldosteronism concerns the results of 2 different operative methods. After preoperative localization of the unilateral solitary tumor 22 patients underwent unilateral adrenalectomy and 26 underwent enucleation of aldosterone-producing adenoma. Both operative methods improved hypertension, hypokalemia, the low urinary sodium-to-potassium ratio, suppressed plasma renin activity, high plasma aldosterone concentration, high urinary aldosterone excretion and high urinary kallikrein excretion in similar orders of magnitude for 5 years. Levels of plasma cortisol and plasma adrenocorticotropic hormone following respective operations were also identical. Five years postoperatively, ambulation and furosemide administration under low sodium diet stimuli remarkably enhanced plasma renin activity and plasma aldosterone concentration in the aldosterone-producing adenoma enucleation group (p < 0.001), almost similar to that of normal subjects but increment magnitudes were slight (p < 0.05 to < 0.01) in the adrenalectomy group. Preoperatively, angiotensin II infusion failed to increase plasma aldosterone concentration in patients with primary aldosteronism. After respective operations, responses of plasma aldosterone concentration to angiotensin II infusion and of plasma cortisol to adrenocorticotropic hormone administration in the aldosterone-producing adenoma enucleation group were more sensitive than those in the adrenalectomy group. There was no remission of recurrent hyperaldosteronism in either group throughout the study. These results suggest that angiotensin II induces aldosterone release by an activation of tumor uninvolved cortical cells and that the enucleation of aldosterone-producing adenoma is more preferable than unilateral adrenalectomy.
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PMID:Therapeutic outcome of primary aldosteronism: adrenalectomy versus enucleation of aldosterone-producing adenoma. 775 16

The present study had two objectives: (1) to provide information on neuroendocrine challenge tests that can lead to diagnostic tests in humans; and (2) to confirm our previous observation that chronic fluoxetine selectively inhibits serotonin (5-HT1A) receptor function. We determined the effect of chronic fluoxetine and desipramine (DMI) on the hormone response to ipsapirone, a 5-HT1A agonist and a potential anxiolytic drug. Ipsapirone increased oxytocin, adrenocorticotropic hormone (ACTH), corticosterone, and prolactin, but not renin or vasopressin concentrations in plasma. Chronic fluoxetine, but not DMI, significantly inhibited the effect of ipsapirone on plasma oxytocin, ACTH and corticosterone concentrations. Chronic fluoxetine also reduced the Bmax for 3H-8-hydroxy-2-(dipropylamino) tetralin (3H-8-OH-DPAT) labelled 5-HT1A receptors in the midbrain. Neither antidepressant altered the density or affinity of 5-HT uptake sites. In conclusion, the present results confirm our previous results using 8-OH-DPAT as a challenge, and suggest that chronic 5-HT uptake inhibition results in adaptive changes leading to decreased function of the 5-HT1A receptor system. Finally, because ipsapirone may be administered to humans, it might be usable to evaluate 5-HT1A receptor function in depressed patients.
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PMID:Attenuation of hormone responses to the 5-HT1A agonist ipsapirone by long-term treatment with fluoxetine, but not desipramine, in male rats. 799 56

The present study investigated the consequences of prenatal cocaine exposure on central serotonin (5-HT) 5-HT1A receptor-mediated function in prepubescent male and female progeny. Pregnant rats received saline or cocaine (15 mg/kg s.c.) twice daily from gestational day 13 through 20. All litters were fostered to nontreated lactating dams. Cocaine did not alter weight gain during pregnancy and did not affect progeny weight at birth or at postnatal day 28. Male and female progeny were tested at a prepubescent age (postnatal day 28) by measuring 1) the stimulation of adrenocorticotropic hormone, corticosterone and renin by a maximally effective dose (0.5 mg/kg s.c.) of the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT); and 2) [3H]8-OH-DPAT-labeled 5-HT1A receptors and [3H]paroxetine-labeled 5-HT uptake sites in hypothalamus, cortex and midbrain. Basal hormone levels were unaffected by prenatal cocaine exposure. However, prenatal cocaine exposure significantly potentiated the adrenocorticotropic hormone (+28%) and renin (+53%) responses to 8-OH-DPAT in male but not female progeny. In contrast, the corticosterone response to 8-OH-DPAT was not significantly altered in either male or female progeny. Likewise, the number of 5-HT1A receptors and 5-HT uptake sites in the cortex, midbrain and hypothalamus were unaffected by prenatal cocaine exposure. These data demonstrate that prenatal cocaine exposure can potentiate brain 5-HT1A receptor-mediated function in progeny and that alterations in hypothalamic 5-HT1A function are gender specific. These data suggest the possibility that prenatal cocaine may increase 5-HT1A receptor function in extrahypothalamic brain regions.
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PMID:Potentiation of 5-HT1A receptor-mediated neuroendocrine responses in male but not female rat progeny after prenatal cocaine: evidence for gender differences. 799 58

Angiotensin converting enzyme plays a key role in the regulation of blood pressure and inhibitors of the enzyme are effective antihypertensive agents. An association between hypertension and alcohol abuse has long been recognized and manipulations of the renin-angiotensin system in laboratory animals has been shown to alter their consumption of ethanol. Procedures that decrease the renin-angiotensin system increase ethanol consumption. Paradoxically, inhibitors of angiotensin converting enzyme also diminish drinking. Several possible explanations for this observation have been proposed. However, observations on the relationship between stress-induced drinking and the antidipsogenic action of a fragment of adrenocorticotropic hormone suggest another possibility: angiotensin converting enzyme may be involved in the metabolism of this peptide and thereby exert an influence on drinking behavior.
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PMID:Angiotensin converting enzyme inhibitors and alcohol abuse. 803 63

This study tested whether a new serotonin (5-HT1B) agonist, 3-(1,2,5,6-tetrahydro-4-pyridyl)-5-propoxy-pyrrolo[3,2-b]pyridine (CP-93,129), could be used to study the potential role of 5-HT1B receptors in the secretion of adrenocorticotropic hormone (ACTH), prolactin, and renin. CP-93,129 has a high affinity for 5-HT1B receptors but low affinity for other 5-HT receptor subtypes. In addition, CP-93,129 does not readily cross the blood-brain barrier. The secretion of ACTH, prolactin, and renin is known to be increased after activation of 5-HT receptors. ICV injections of CP-93,129 (100 micrograms/kg) increased the plasma concentrations of ACTH, prolactin, and renin. CP-93,129 also increased blood pressure and reduced heart rate. To determine whether these effects of CP-93,129 are centrally mediated, we compared them with IP injection of the same dose of CP-93,129. IP-injected CP-93,129 did not alter blood pressure or heart rate and did not elevate plasma prolactin and renin concentrations. To determine whether 5-HT1B receptors mediate the central effects of CP-93,129, rats were pretreated with the 5-HT antagonists l-propranolol or metergoline prior to ICV injections of doses of CP-93,129 (0-100 micrograms/kg). The 5-HT1A/1B/2A/2C antagonist metergoline (0.5 mg/kg, IP) failed to inhibit the CP-93,129-induced elevation of ACTH, prolactin, or renin concentrations. In contrast, the 5-HT1A/1B/beta antagonist l-propranolol (20 micrograms/kg, ICV) inhibited the renin but not the ACTH or prolactin responses to ICV CP-93,129.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ICV injection of the serotonin 5-HT1B agonist CP-93,129 increases the secretion of ACTH, prolactin, and renin and increases blood pressure by nonserotonergic mechanisms. 809 Aug 11

This study was performed to test the hypothesis that smaller reflex increases in vasopressin, cortisol, adrenocorticotropic hormone (ACTH), and angiotensin II (ANG II) concentrations are produced by hemorrhage in pregnant compared with nonpregnant conscious dogs. Equivalent hemorrhages (1% of the initial blood volume per minute) produced larger decreases in arterial pressure [P < 0.01; 107 +/- 6 to 73 +/- 10 mmHg (pregnant); 109 +/- 6 to 90 +/- 5 mmHg (nonpregnant)] but produced similar increases in plasma vasopressin concentration in the pregnant animals. As a result, the slope of the arterial pressure-to-vasopressin relationship was reduced (P < 0.05). During pregnancy, smaller increases in plasma cortisol concentration and heart rate were also produced for a given decrease in arterial pressure, but the relationship between pressure and ACTH was not significantly affected. In contrast, higher levels of plasma renin activity and plasma ANG II concentration were achieved in the pregnant dogs. In general, the relationships between plasma hormone levels and either left or right atrial pressure were not significantly altered. These results indicate that reflex increases in heart rate, vasopressin, and cortisol concentration are attenuated in pregnant dogs and that this attenuation may contribute to the inability of pregnant animals to achieve normal cardiovascular homeostasis during hemorrhage.
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PMID:Hemorrhage decreases arterial pressure sooner in pregnant compared with nonpregnant dogs: role of baroreflex. 818 41

To evaluate the inhibitory effect of hypoxia and atrial natriuretic peptide (ANP) on aldosterone secretion, 11 healthy male subjects were infused with 5 ng.kg-1 x min-1 ANP or placebo. The subjects were exposed in a stepwise fashion to incremental hypobaric hypoxia, which decreased arterial oxygen saturation to 79 +/- 2% in the placebo and 84 +/- 2% in the ANP condition (P < 0.05). In the placebo condition, the plasma ANP concentration increased from 13.8 +/- 1.0 to 19.6 +/- 2.3 pmol/l (P < 0.01) at the lowest barometric pressure. Plasma renin activity did not change, whereas the plasma aldosterone levels increased consequent to the increase of plasma adrenocorticotropic hormone (ACTH). Continuous infusion of ANP increased the plasma levels twofold (P < 0.001) and the level of guanosine 3',5'-cyclic monophosphate threefold (P < 0.001). However, the plasma aldosterone concentrations were not different in the two experimental conditions. Administration of supplementary oxygen significantly decreased ACTH to baseline values (P < 0.01) together with a decrease in aldosterone. Free water clearance (P = 0.05) but not sodium excretion (P = NS) increased during continuous ANP infusion. The data indicate that the aldosterone secretion in hypoxia is not inhibited by (patho)physiological plasma ANP levels. The inhibition of aldosterone secretion may well be explained by a direct effect of hypoxia on the adrenal cells. ACTH is a major stimulus of aldosterone secretion in hypoxia, which overrides the natriuretic effect of ANP.
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PMID:Effects of hypoxia and atrial natriuretic peptide on aldosterone secretion in healthy subjects. 822 50

This study was performed to test the hypothesis that thromboxane A2 stimulates increases in fetal adrenocorticotropic hormone (ACTH), vasopressin, or renin secretion and affects fetal cardiovascular function by an action on the fetal central nervous system. We infused a stable synthetic analogue of thromboxane A2, U-46619, into one common carotid artery or inferior vena cava or infused saline into one common carotid artery in chronically catheterized fetal sheep between 127 and 140 days gestation. We found that intracarotid but not intravenous infusions of U-46619 at a rate of 750 ng/min stimulated increases in fetal plasma ACTH concentration. Infusions of U-46619 at both sites increased fetal blood pressure; the infusion into the carotid arterial blood produced a more rapid increase in blood pressure and a significant decrease in central venous pressure. None of the infusions altered plasma vasopressin concentration or plasma renin activity, blood gases, hematocrit, or plasma cortisol concentration. We conclude that thromboxane A2 stimulates fetal ACTH, but not vasopressin or renin, secretion via an action within the area perfused by carotid arterial blood. Thromboxane A2 increases blood pressure via an action at the fetal central nervous system, as well as via a direct vasoconstrictor action in the systemic circulation.
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PMID:Fetal ACTH and blood pressure responses to thromboxane mimetic U-46619. 823 57


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