Effect of methylprednisolone upon arterial pressure and the renin angiotensin system in the rat

1975 ◽  
Vol 228 (2) ◽  
pp. 613-617 ◽  
Author(s):  
LR Krakoff ◽  
R Selvadurai ◽  
E Sutter
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Significant Fall ◽  
Arterial Blood ◽  
Methylprednisolone Treatment

The effect of methylprednisolone or deoxycorticosterone upon systemic arterial blood pressure and components of the renin-angiotensin system was studied in the rat. Rats maintained on regular diets given methylprednisolone suspension 20 mg/kg body wt demonstrated a significant increase in arterial pressure of + 37 plus or minus 5 mmHg, mean plus or minus SE, over a 2-wk period, whereas those treated with DOC and untreated controls showed no significant change. On normal diets, plasma renin concentration (PRC) of methylprednisolone-treated rats was significantly higher than that of DOC-treated rats. Methylprednisolone treatment also resulted in a significant elevation of plasma renin substrate concentration (PRS). Calculated plasma renin activity (PRA) was highest in methylprednisolone-treated rats, significantly above that of the DOC and no-steroid groups. NaCl supplementation resulted in a significant fall in PRC and PRA in all three groups; however, PRS remained significantly above normal in the methylprednisolone-treated rats. The pressor effect of angiotensin II was slightly increased in methylprednisolone-treated rats. Infusion of [Sar1,Ala8]angiotensin II (P-113) in methylprednisolone-treated rats resulted in a significant fall in diastolic arterial pressure. The results imply that methylprednisolone hypertension in the rat may be in part angiotensin dependent.

Renin-angiotensin system in hypophysectomized rats. I. Control of blood pressure

1984 ◽  
Vol 246 (1) ◽  
pp. E84-E88
Author(s):  
C. D. Simon ◽  
T. W. Honeyman ◽  
J. C. Fray
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Hormone Administration ◽  
Hypophysectomized Rats

The mechanisms whereby the pituitary gland maintains arterial pressure were investigated in rats. The arterial pressure in hypophysectomized rats was 30 mmHg below normal. Saralasin or captopril caused a further fall of 25 and 30 mmHg, respectively, suggesting that the renin-angiotensin system plays a role in blood pressure maintenance in hypophysectomized rats. Growth hormone administration to hypophysectomized rats increased the arterial pressure, but pretreatment with captopril prevented the effect. Plasma renin activity and basal renin secretion (in vitro) was normal in hypophysectomized rats despite a twofold greater renal renin content. Secretory responsiveness to isoproterenol and calcium omission was lower in hypophysectomized rats. It is concluded that the renin-angiotensin system plays a role in maintaining arterial blood pressure in hypophysectomized rats although the responsiveness of the system may be decreased.

Renin–Angiotensin System in Mild Essential Hypertension. the Functional Significance of Angiotensin II in Untreated and Thiazide-Treated Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 319s-321s ◽  
Author(s):  
H. Ibsen ◽  
A. Leth ◽  
H. Hollnagel ◽  
A. M. Kappelgaard ◽  
M. Damkjaer Nielsen ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Functional Significance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Twenty-five patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. 2. Basal and post-frusemide values for plasma renin concentration and plasma angiotensin II concentration did not differ markedly from reference values in 25 40-year-old control subjects. In the untreated, sodium replete state saralasin infusion (5·4 nmol min−1 kg−1) produced an increase in mean arterial pressure in the patient group as a whole. 3. Twenty-one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months. Pre-treatment, frusemide-stimulated plasma renin concentration and plasma angiotensin II, and values during thiazide treatment were higher in ‘non-responders’ (n = 10) to hydrochlorothiazide treatment than in ‘thiazide-responders’ (n = 11). During thiazide therapy, angiotensin II blockade induced a clear-cut decrease in mean arterial pressure in all ‘thiazide-nonresponders’ whereas only four out of 11 ‘thiazide-responders’ showed a borderline decline in mean arterial pressure. 4. The functional significance of the renin—angiotensin system in mild essential hypertension emerges only after thiazide treatment. Thiazide-induced stimulation of the renin—angiotensin system counter-balanced the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of the renin—angiotensin system determined the blood pressure response to thiazide treatment.

Comparison of hormonal responses to hypotension in mature and immature fetal lambs

1988 ◽  
Vol 255 (1) ◽  
pp. R67-R72 ◽  
Author(s):  
N. M. Rawashdeh ◽  
N. D. Ray ◽  
D. K. Sundberg ◽  
J. C. Rose
Keyword(s):  
Arterial Pressure ◽  
Renin Angiotensin System ◽  
Blood Gases ◽  
Plasma Renin ◽  
Arterial Blood Gases ◽  
Hormonal Responses ◽  
Angiotensin System ◽  
Induced Hypotension ◽  
Functional Deficit ◽  
Arterial Blood

We studied norepinephrine (NE) and plasma renin activity (PRA) responses to sodium nitroprusside (NP)-induced hypotension in seven chronically catheterized fetal lambs 0.79-0.94 gestation (mature) and in seven fetuses 0.64-0.72 gestation (immature) 4 or 5 days after surgery. We infused intravenously 5% dextrose in water (DW) or NP in DW to reduce arterial pressure 30% in fetuses for 10 min. Initial infusion choice was random, and the two infusions were separated by 24-48 h. In both groups, basal NE levels were similar and doubled in response to hypotension. In mature fetuses, PRA basal levels were 6.89 +/- 1.80 ng.ml-1.h-1 and increased two- to threefold with hypotension. In immature fetuses, PRA basal levels were 2.42 +/- 0.86 ng.ml-1.h-1 and did not change with hypotension. No changes were observed with DW infusion in either group. Arterial blood gases were normal and remained unchanged. We conclude that in the lamb fetus, NE responses to hypotension are present before and are independent of the development of PRA responses and that before 0.72 gestation there is a functional deficit in the renin-angiotensin system.

Postnatal development of the renin-angiotensin system in rats

1980 ◽  
Vol 238 (5) ◽  
pp. R432-R437 ◽  
Author(s):  
K. B. Wallace ◽  
J. B. Hook ◽  
M. D. Bailie
Keyword(s):  
Steady State ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Neonatal Rat ◽  
Postnatal Life ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Age Related

The purpose of this investigation was to correlate the development of the various enzyme activities associated with the renin-angiotensin system with age-related differences in the steady-state concentrations of angiotensin I (AI) and II (AII). Angiotensin was quantified by radioimmunoassay. Plasma renin activity and concentration increased between birth and 3 wk of age, and declined thereafter to adult values. Renal renin content, on the other hand, increased throughout the first 6 wk of postnatal life. The concentration of AII in plasma also increased following birth; however, maximum concentrations were not attained until 5 wk of age. In contrast, plasma AI did not increase between 3 and 6 wk of age. These data suggest that the steady-state concentration of AII in neonatal rat plasma may be partially limited by the low plasma renin substrate concentration. The increase in AII between 3 and 6 wk of age may reflect the increasing converting enzyme activity.

Methods for serial study of renin-angiotensin system in the unanesthetized rat

1975 ◽  
Vol 228 (2) ◽  
pp. 369-375 ◽  
Author(s):  
JS Carvalho ◽  
R Shapiro ◽  
P Hopper ◽  
LB Page
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Angiotensin I ◽  
Ether Anesthesia ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Improved Technique

Micromethods for measurement of plasma renin concentration (PRC) and plasma renin-substrate concentration (PSC) have been developed for rat plasma with radioimmunoassay of angiotensin I. An improved technique for aortic implantation of plastic cannulas was developed for use in experiments 1-2 wk in duration. The effects on components of renin system of anesthesia and tail cutting were studied. Arterial blood was sampled through cannulas without animal manipulation. PRC varied little in unanesthetized rats, was moderately and variably increased during pentobarbital anesthesia, and was markedly and consistently elevated during ether anesthesia. PSC was unchanged during anesthesia. PRC was increased in blood obtained by tail cutting within 1-2 min after cutting. With the use of the methods and techniques described here serial studies of the renin system in plasma of unanesthetized rats are shown to be feasible. A role for the sympathetic nervous system in the mediation of renin secretion by ether is proposed.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

Splanchnic vasoconstriction in heat-stressed men: role of renin-angiotensin system

1982 ◽  
Vol 52 (6) ◽  
pp. 1438-1443 ◽  
Author(s):  
P. Escourrou ◽  
P. R. Freund ◽  
L. B. Rowell ◽  
D. G. Johnson
Keyword(s):  
Heat Stress ◽  
Arterial Pressure ◽  
Nervous Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Sympathetic Nervous Activity ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Norepinephrine Concentration

We conducted a two-part study to determine whether the renin-angiotensin system contributes to the rise in splanchnic vascular resistance (SVR) during heat stress (rectal temperature was raised 1 degree C). In experiment 1 (control) seven men on a normal salt diet were directly heated (water-perfused suits) for 40–50 min. Arterial pressure (85 Torr) was unchanged; plasma renin activity (PRA) rose from 102 to 239 ng angiotensin I.100 ml-1.3 h-1; and SVR increased 73% (from 63 to 109 units). Experiment 2 was a repetition of experiment 1 on the same subjects, except that propranolol (10 mg iv) was given at the onset of heating to block renin release. Propranolol attenuated the rise in heart rate and reduced mean arterial pressure from 82 to 72 Torr; it blocked the rise in PRA with heating in two subjects, reduced it in three, but increased it in two. Although changes in SVR paralleled those in PRA in three subjects, SVR still rose 60% (from 58 to 99 units) after PRA rise was blocked. In both experiments, plasma norepinephrine concentration rose indicating increased sympathetic nervous activity. During mild heat stress, increased PRA is not a major factor in the increase of SVR.

Renin-angiotensin system in hypothyroid rats: effects of potassium iodide and triiodo-L-thyronine

1984 ◽  
Vol 105 (4) ◽  
pp. 505-510 ◽  
Author(s):  
E. Jiménez ◽  
M. Montiel ◽  
J. A. Narváez ◽  
M. Morell
Keyword(s):  
Plasma Renin Activity ◽  
Potassium Iodide ◽  
Renin Angiotensin System ◽  
Kinetic Studies ◽  
Plasma Renin ◽  
The Other ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Previously Treated

Abstract. Kinetic studies of the renin-angiotensin system (RAS) were carried out by measuring plasma renin activity (PRA), plasma renin concentration (PRC) and plasma renin substrate (PRS). Changes in this system were studied during hypothyroidism, after administration of propylthiouracil (PTU), and in thyroidectomized rats. A significant decrease in PRA and PRC was observed in those animals previously treated with PTU. However, a significant increase in PRC, and a decrease in PRS, were found in T animals, but no changes in PRA were observed. In these animals, after daily administration of potassium iodide for I week (T+KI), no changes in RAS were observed in comparison with T rats. Nevertheless, administration of daily doses of triiodo-ithyronine (T+T3) induced a significant increase in PRA, leaving PRC unaltered. In this case the changes in PRA were related to the increase in PRS after T3 treatment. These results suggest that two different mechanisms were involved in renin release, one activated in T rats and the other in pharmacological hypothyroidism.

Studies on the human ovarian renin-angiotensin system: optimization of assay methodology and effects of follicular stimulants

1990 ◽  
Vol 127 (3) ◽  
pp. 513-521 ◽  
Author(s):  
J. M. Brameld ◽  
F. Broughton Pipkin ◽  
E. M. Symonds
Keyword(s):  
Follicular Fluid ◽  
Ovarian Stimulation ◽  
Clomiphene Citrate ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
System Optimization ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Substrate Concentrations

ABSTRACT The renal and genital tracts share a common embryological origin; it is thus not surprising that tissues from both can synthesize renin. Preliminary studies showed extremely high concentrations of renin in follicular fluid (FRC) following ovarian stimulation for in-vitro fertilization. This necessitated complete revalidation of the renin assays and showed that data obtained using commercial kits were invalid. An assay protocol was developed using a 1:2 dilution of follicular fluid taken into EDTA (0·3 mol/l) and o-phenanthroline (0·05 mol/l). The assay was performed at pH 7·5 in the presence of excess exogenous (sheep) renin substrate, with incubation periods of 5, 10 and 15 min at 37 °C. This protocol resulted in the linear generation of angiotensin I (AI). Activation of inactive renin was performed using eightfold more trypsin than was required for plasma samples. Follicular renin substrate concentrations (FRS) were measured using the same assay methodology as used for measurement of plasma renin substrate concentrations (PRS). Storage of samples at −18 °C for up to 2 months was found not to affect the FRC, although repeated freeze-thaw cycles did. FRC and plasma renin concentrations (PRC) were very similar in 25 unstimulated control women, studied in the follicular phase of the menstrual cycle. Trypsin activation increased follicular total renin concentration (FTRC) more than plasma total renin concentration (PTRC) (P< 0·0001). FRS was slightly higher than PRS (P<0·02). Ovarian stimulation with clomiphene citrate (CC; six women) was without effect on these parameters. However, hyperstimulation with CC, human menopausal gonadotrophins (hMG) and human chorionic gonadotrophin (hCG) resulted in substantial increments in FRC and FTRC (P< 0·0001 for both) and somewhat smaller rises in PRC and PTRC (P<0·05; P < 0·0005). There was also a small rise in PRS (P< 0·0002), but no change in FRS. Treatment with buserelin, hMG and hCG was associated with similarly large increases in renin concentrations, and also increases in both FRS and PRS (P< 0·003; P<0·007) in comparison with samples from women stimulated with CC, hMG and hCG. Increased plasma renin activity has previously been reported in stimulated ovarian follicular fluid. Our data show clearly that this is primarily due to a rise in FRC and FTRC and not to a rise in FRS. The use of the anti-oestrogen CC alone for ovarian stimulation was without effect on the follicular renin-angiotensin system. Thus we suggest that it is the gonadotrophins themselves which stimulate renin production, presumably by the theca cells. The much smaller rise in PRC and PTRC may reflect the effects of an overspill into the systemic circulation or, less likely, effects of the gonadotrophins on renal renin production. There is no evidence for this latter suggestion. FRS was increased only slightly by ovarian stimulation and must be presumed to be rate-limiting in the generation of AI. Journal of Endocrinology (1990) 127, 513–521

scholarly journals Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy

1999 ◽  
Vol 160 (1) ◽  
pp. 43-47 ◽  
Author(s):  
H Kobori ◽  
A Ichihara ◽  
Y Miyashita ◽  
M Hayashi ◽  
T Saruta
Keyword(s):  
Angiotensin Ii ◽  
Thyroid Hormone ◽  
Cardiac Hypertrophy ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin ◽  
Renin Mrna

We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin-angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague-Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily i.p. injection of thyroxine (0.1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri-iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0.12+/-0.03 and 0.15+/-0.03 microgram/h per liter, 126+/-5 and 130+/-5 ng/l respectively) (means+/-s.e.m.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5.0+/-0.5 vs 3.5+/-0.1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74+/-2 vs 48+/-2%, 6.5+/-0.8 vs 3.8+/-0.4 ng/h per g, 231+/-30 vs 149+/-2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.

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