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Biomedical subjects

J Menard

Publications and source records attributed to J Menard.

At least 145 records · Page 8Linked to original sources
PubMed1983

[A simple diagnostic test for primary hyperaldosteronism].

Plasma aldosterone levels were measured as part of two suppression tests in 31 hypertensive patients on normal sodium diet and without recent treatment. Thirteen patients had essential hypertension, 6 had probable bilateral adrenal hyperplasia and 12 had confirmed Conn's adenoma. In the first test, aldosterone levels were measured in the supine patients, then after infusion of 2 litres of isotonic saline over 2 hours. In the second test, aldosterone levels were measured before and 3 hours after oral administration of Captopril 1 mg/kg. Plasma aldosterone values superior to 360 pmol.l-1 after sodium load or to 665 pmol.l-1 after Captopril were characteristic of primary hyperaldosteronism due to adenoma. The test using Captopril has the advantages of being rapid, of avoiding acute blood volume expansion and of being applicable to all forms of hypertension, including severe ones.

Adrenal Glands↗
PubMed1983

Immunocytochemical localization of angiotensinogen in rat liver and kidney.

The renin substrate, angiotensinogen, was localized by immunocytochemistry in liver and kidney of normal rats by the use of an antiserum directed against pure rat angiotensinogen. This substrate was also examined in rats after bilateral nephrectomy, which is known to increase plasma angiotensinogen, and in rats treated with colchicine, which inhibits serum protein secretion. In normal rat liver, light microscopy showed the presence of immunoreactive material in a very few cells. The number of stained hepatocytes rose in rats treated with colchicine or after bilateral nephrectomy. Immuno-staining increased further when rats were both nephrectomized and colchicine treated. In the kidney, angiotensinogen was specifically located as granular formations in nephrocytes of the proximal tubule but never in the granular cells of the juxtaglomerular apparatus. The localization of these granular formations under the brush border suggests that angiotensinogen is reabsorbed from the glomerular ultrafiltrate rather than synthesized in the kidney.

Angiotensinogen↗
PubMed1983

Fetal growth retardation in gestational hypertension: relationships with blood pressure levels and the time of onset of hypertension.

To evaluate the effects of gestational hypertension on fetal growth, we studied the standardized records of 2996 single live-birth pregnancies. Mothers all had documented diastolic blood pressure of less than 85 mmHg before the 16th wk of amenorrhea and no history of pre-pregnancy hypertension or kidney disease. Diastolic blood pressure readings exceeding 84 mmHg were found later in pregnancy in 38.4% of the mothers, and were associated with an increased number of small-for gestational-age infants: 3.2% in mothers whose diastolic blood pressure had never reached 85 mmHg, 6.3% when peak diastolic blood pressure had been in the 85-94 mmHg range, and 8.5% when it had exceeded 94 mmHg (p less than 0.01). In mothers who had had one or more diastolic readings of more than 84 mmHg, and for all peak diastolic pressures, the rate of small-for-gestational-age infants was higher when hypertension had begun early in third trimester (between the 27th and 36th wk), than in the second trimester or later than the 35th wk (10.2% compared to 5.6 and 6.1% respectively, p = 0.02). This temporal reinforcement of the adverse fetal effects of hypertension when it began in the early third trimester was not explained by differences in the incidence of proteinuria or in maternal age, parity, obstetric history or smoking habits.

Adult↗
PubMed1983

Renal arteriovenous fistula: a model for renovascular hypertension in rat.

Renal arteriovenous fistula (RAVF) was created in the rat. For this purpose the left renal artery and vein were connected by a latero lateral anastomosis. This operation was performed in 40 rats and 12 animals were sham operated. All these animals were subsequently reoperated after 4 weeks to check the fistula and the kidney. Eleven among the 40 operated rats died during or after the surgery. In 16 others animals hypertension developed. Their blood pressure was 161 +/- 4.3 mm. Hg at 4 weeks vs. 105 +/- 1.65 mm. Hg before surgery. All these animals had after 4 weeks a permeable fistula and an atrophic but nonnecrotized left kidney (kidney weight was 0.56 +/- 0.33 gm. vs. 1.32 +/- 0.22 gm. for the sham operated group). They underwent a left nephrectomy without closure of the fistula and subsequently their blood pressure fell back to normal values 120 +/- 2.9 mm. Hg 2 weeks after nephrectomy). In the removed kidney, renal renin content per mg. of protein was found to be higher than in the kidney of the sham operated animals (28.5 +/- 7.9 vs. 0.66 +/- 0.2 micrograms. AI/mg. protein/hour). In 13 other animals the blood pressure remained normal after the initial surgery. These animals had a permeable fistula but a necrotic left kidney. It is concluded that RAVF can induce hypertension in the rat. This hypertension only develops when the ipsilateral kidney remains vascularized and disappears when this kidney is removed without closure of the fistula. Since the renin content in the kidney distal to the shunt was higher than in the kidney of the sham operated rats and since there was a positive correlation between renal renin content and blood pressure in hypertensive animals, it is suggested that an activation of the renin angiotensin system in the ipsilateral ischemic kidney is responsible for hypertension. RAVF therefore appears to be an experimental model for renovascular hypertension in rats.

Animals↗
PubMed1983

Regulation of kallikrein and renin release by the isolated perfused rat kidney.

Rat kidneys perfused in vitro released kallikrein in urine, and renin and kallikrein in the perfusate. The kallikrein was characterized by its kininogenase activity and released bradykinin from bovine and dog substrates. Inactive trypsin activatable kallikrein was present in both perfusate and urine. Kallikrein secretion in urine was influenced by changes in perfusion pressure (PP). Raising the PP strikingly increased urinary kallikrein and lowering PP reduced it. Urinary water and electrolyte output were augmented to the same extent by furosemide and mannitol administration as by raising the PP, but neither drug affected kallikrein. Isoproterenol stimulated the release of renin but not kallikrein. Stopping the oxygen supply to the perfusate suppressed kallikrein secretion in urine and renin release in the perfusate. The kidneys released ten times less kallikrein in the perfusate than in urine, and perfusate kallikrein was not influenced by changes in PP. It is concluded that in this model, changes in PP and/or renal blood flow and/or oxygen supply regulate kallikrein secretion in urine, but that this secretion is unaffected by changes in urinary output. We also conclude that kallikrein release in urine and renin release in perfusate are regulated simultaneously by renal hemodynamic changes but are not affected concomitant by beta-adrenergic stimulation or changes in distal urine composition.

Animals↗
PubMed1983

Abnormalities of renin-containing cells in human glomerular and vascular renal diseases.

The distribution of renin was investigated by immunofluorescence in human kidney biopsy specimens (27 patients with lipoid nephrosis, 39 with Berger disease, 17 with membranous glomerulonephritis, 5 with thrombotic microangiopathy, and 7 with malignant nephroangiosclerosis). A semiquantitative assessment was carried out. Two ratios were found significatively increased in the study groups as compared with the control group: JGA + and JGA ++ which expressed, respectively, the number of fluorescent JGA in relation to the number of glomerular sections and the number of fluorescent JGA with more than six renin-containing cells (RCC) in relation to the number of immunoreactive JGA. Highest values were observed in patients with thrombotic microangiopathy and malignant nephroangiosclerosis (P less than 0.001). The above immunomorphological parameters were correlated with clinical and laboratory data. A positive dependency was found between JGA + and JGA ++ ratios and a low sodium diet, diuretic therapy and serum creatinine. A negative dependency was seen in the albumin and hemoglobin serum levels. No correlation was found with blood pressure values. These observations suggested that decreased plasma volume and impaired renal function could be factors leading to an increased renin production in the kidney.

Adolescent↗
PubMed1983

Synthesis and release of immunoreactive angiotensinogen by rat liver slices.

Hepatic storage and secretion of angiotensinogen was studied using rat liver slices and a new direct angiotensinogen RIA. This assay permitted the demonstration of a significant hepatic storage of angiotensinogen, largely underestimated until now by the enzymatic method of angiotensinogen measurement. Angiotensinogen release by rat liver slices was linear with time and was associated with a significant increase in hepatic content of angiotensinogen. The measurement of both release and changes in hepatic content permitted the measurement of de novo synthesis of angiotensinogen by rat liver slices in vitro. Both hepatic content and release of angiotensinogen were decreased by thyroidectomy and increased by ethinyl estradiol, dexamethasone, thyroid hormones, and binephrectomy.

Angiotensinogen↗
PubMed1982

[Role of vasopressin in arterial hypertension].

On isolated arteriole preparations vasopressin behaves as an extremely potent vasoconstrictor. In healthy animals and man its pressor effect is counteracted by several compensatory mechanisms, including stimulation of the baroreceptor reflex with reduction of sympathetic activity, decrease in renin secretion, sodium loss and reduction of vascular response to vasopressor agents. Alterations of these mechanisms unmask the hypertensive effect of vasopressin as shown by several experimental hypertension models in animals. In human pathology vasopressin has been shown to be a good indicator of the severity pf arterial hypertension, but its role in that disease will only be determined when vascular antagonists of vasopressin devoid of paryial agonistic activity become available.

Animals↗
PubMed1982

Direct radioimmunoassay of rat angiotensinogen and its application to rats in various endocrine states.

1. Antibodies were raised in rabbits against pure rat angiotensinogen. The antisera obtained were highly specific for rat angiotensinogen and did not bind hog, dog, rabbit, monkey or human angiotensinogen. They did not cross-react with angiotensin I, angiotensin II or synthetic hog tetradecapeptide renin substrate. However, rat des-angiotensin I-angiotensinogen cross-reacted 100% with the angiotensinogen antibody. 2. A direct radioimmunoassay for rat angiotensinogen in plasma was developed and this enable 5 fmol of this protein to be detected. Comparison of the amounts of angiotensinogen determined by the indirect and direct assay systems indicated a 1:1.2 ratio for normal rats and rats in various endocrine states, except for adrenalectomized animals. In the latter, the angiotensinogen level measured by direct radio-immunoassay was four times that obtained by indirect assay. 3. The presence of a large amount of des-angiotensin I-angiotensinogen in adrenalectomized rat plasma is discussed.

Angiotensinogen↗
PubMed1982

Antihypertensive effect of diacetolol in essential hypertension.

1 Diacetolol is the N-acetylated metabolite of acebutolol and possesses beta-adrenergic receptor blocking properties. 2 Its antihypertensive action was assessed in accordance with a double-blind randomised cross-over scheme in 17 patients with moderate essential hypertension previously well controlled with acebutolol. 3 Significant reductions in lying mean arterial blood pressure were observed with daily doses of 200 mg (- 9%), 400 mg (- 10%) and 800 mg (- 14%), and were associated with significant decreases in heart rate and plasma renin activity. 4 The diacetolol mean plasma level measured 8 to 10 h after drug ingestion was proportional to the dose (207 +/- 27, 394 +/- 63 and 823 +/- 135 ng/ml for respectively 200, 400 and 800 mg/day).

Acebutolol↗
PubMed1982

Biochemical and immunological characterization of ectopic tumoral renin.

Biochemical and immunological characteristics of renin secreted by two malignant renin-secreting tumors [pulmonary (PT) and paraovarian (POT)] were studied. They both contain inactive renin (IR), as renin activity of tumoral extracts was able to be increased after acid activation or trypsin treatment (10.1 to 20.8 Goldblatt units/g tissue for PT and 1.4 to 3.71 for POT). Renin activity after activation reached the value obtained by direct RIA of human renin (23 and 3.4, respectively), as both forms are recognized by renin antiserum. Both enzymatic activities could be completely inhibited by renin antiserum. Displacement curves for the two tumoral renins paralleled the MRC renin in the direct RIA. After chromatography on affigel blue, active renin was not bound to the gel, and inactive renin eluted only with 1 M NaCl. On pepstatin A Sepharose and CBL-pepstatin Sepharose (an N-modified-pepstatin), a separation of the two forms of pulmonary renin was obtained; inactive renin eluted with breakthrough proteins, whereas active renin was strongly bound to the gel. After this affinity chromatography, the molecular weights of inactive and active renin, determined on Ultrogel, were very close (46,000 and 42,500). We conclude that 1) ectopic renin in these cases in similar to the renal enzyme; 2) renin can be secreted in an inactive form, supporting the hypothesis of an inactive initial state of renin; and 3) molecular weight differences between the two forms are very slight.

Adenocarcinoma↗
PubMed1982

Human chorionic cells in primary culture: a model for renin biosynthesis.

Amnion and chorion cells from human fetal membranes have been cultured. Chorionic cells secrete renin whereas amnionic cells do not. Renin is secreted by chorionic cells as an inactive form that can be activated by trypsin treatment or acid dialysis. The antigenic and enzymatic properties of activated chorionic renin and kidney renin are similar. Incorporation of [35S]methionine in the culture demonstrates that chorionic renin is secreted as a high molecular weight form, 54K. This 54K inactive renin could represent the proenzyme.

Amnion↗
PubMed1982

In vitro biosynthesis of human renin: evidence for a high molecular weight form.

Primary cultures of human chorionic cells have been developed. They secrete an inactive form of renin which can be activated by trypsin treatment. In biosynthesis experiments forming labelled renin the inactive renin exhibited a molecular weight (54 KD) higher than active kidney renin (44 KD). The same high molecular weight renin was obtained during biosynthesis experiments performed on tissue slices of human infarcted kidney. Therefore it is postulated that 54 KD biosynthetized renin might be the precursor of active renin.

Cells, Cultured↗
PubMed1982

Acute antihypertensive and hormonal effects of a calcium antagonist in essential hypertension.

In a double-blind versus placebo preliminary study conducted in seven mildly hypertensive patients, the 10-mg capsule form of nifedipine was able to reduce significantly systolic and diastolic blood pressure (-14%) for 3 h. In a single-dose, cross-over study, captopril (1 mg/kg) and nifedipine (20 mg) significantly reduced blood pressure in 12 patients with moderate essential hypertension, but the mean maximum arterial pressure reduction was faster and greater with nifedipine than with captopril (-23 +/- 2% at 37 +/- 15 min and -17 +/- 1% at 86 +/- 25 min, respectively). Nifedipine did not significantly alter the renin angiotensin aldosterone system in supine and upright positions, and the blood pressure drop it induced was not related to the initial level of activation of that system. Associated with the stimulation of the sympathetic nervous system, an increased release of vasopressin was noted during nifedipine administration. Finally, nifedipine, a calcium antagonist, was a potent antihypertensive drug through its vasodilating properties. It provoked specific hormonal alterations, i.e., stimulation of catecholamines and vasopressin release, whereas the renin angiotensin aldosterone system was not significantly altered.

Antihypertensive Agents↗