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Biomedical subjects

H D Itskovitz

Publications and source records attributed to H D Itskovitz.

At least 55 records · Page 3Linked to original sources
PubMed1977

Patterns of blood pressure in Milwaukee.

Blood pressure measurements were obtained among 92,074 persons in Milwaukee between 1974 and 1976 by the Milwaukee Blood Pressure Program. Systolic hypertension was more prevalent in young white men than blacks below 25 years of age, was more common in middle-aged blacks than whites, and was equally prevalent among all persons past 65 years. Diastolic hypertension was more prevalent in blacks than whites of all ages. Whereas the prevalence of systolic hypertension in the population increased with age and was present in a majority or near majority of persons past 65 years, the prevalence of diastolic hypertension rose until the sixth decade, after which it declined. Hypertension was primarily of a diastolic variety in young blacks, whereas systolic hypertension was a prominent feature in young whites.

Adolescent↗
PubMed1977

(Des-Asp1) angiotensin I: a study of its pressor and steroidogenic activities in conscious rats.

The steroidogenic and pressor activities of the nonapeptide (des-Asp1) angiotensin I [(des-Asp)-AI] were tested in conscious rats. (des-Asp)-AI caused dose related increases in mean arterial pressure (MAP), serum aldosterone, and serum corticosterone in doses between 3 and 3,000 ng/kg/min. (des-Asp)-AI was 14% as potent as angiotensin I and angiotensin II and 60% as potent as (des-Asp1) angiotensin II [des-Asp)-AII] in raising MAP. (des-Asp)-AI was less active than AI, AII, or (des-Asp)-AII in causing increased release of aldosterone, possessing only 8%, 11%, and 17% of the potency of AII, (des-Asp)-AII, and AI, respectively. Each of these angiotensin peptides was equally potent in elevating serum corticosterone levels. Infusions of a nonapeptide inhibitor of converting enzyme (CEI, 0.5 mg/kg/min iv) did not alter control MAP or blood pressure responses to AII or (des-Asp-)-AII but inhibited equally the blood pressure effects of AI and (des-Asp)-AI. CEI also inhibited the ability of (des-Asp)-AI (67% inhibition) and AI (34% inhibition) to increase the serum aldosterone concentration, but had no effect on basal aldosterone levels. These data indicate that (des-Asp)-AI has pressor and steroidogenic effects, but requires conversion to (des-Asp)-AII for a major portion of its activity. These results further substantiate the hypothesis that (des-Asp)-AII, recently recognized as a hormone of the renin-angiotensin system, may be produced without the formation of AII as an intermediate and provide in vivo evidence for the conversion of (des-Asp)-AI to (des-Asp)-AII.

Aldosterone↗
PubMed1976

Effect of histamine and antihistamines on renal hemodynamics and functions in the isolated perfused canine kidney.

Histamine was infused intra-arterially (10-40 mug/min) into isolated blood perfused canine kidneys while functional and hemodynamic parameters were monitored. When perfusion pressure (PP) was kept constant during the infusion of histamine, renal blood flow (RBF) increased from 137 +/- 9 to 181 +/- 9 ml/min (P less than .001). A greater increase in RBF occurred to the inner renal cortex than the outer renal cortex as measured by radioactive microspheres. The fractional outer/inner cortical blood flow changed from 79:21 before histamine to 74:26 during its infusion (P less than .001). Histamine did not alter creatinine clearance (Ccr), urine volume (V), sodium excretion (UNaV) or the fractional excretion of sodium (FENa) or water (FEH20) under these conditions. When renal blood flow was held constant during the infusion of histamine, PP decreased from 126/106 +/- 2 to 100/81 +/- 2 mm Hg (P less than .001). This resulted in a reduction of absolute outer cortical (outer/inner) changed from 77:23 before histamine to 72:28 during its infusion (P less than .001). In contrast to the effects of histamine at constant PP, CCr, V, UNaV, FENa, and FEH20 were decreased when histamine infusion reduced the PP. Administration of the H1 receptor antagonist, diphenhydramine, blocked the hemodynamic effects of histamine whereas the administration of an H2 receptor antagonist, metiamide, did not alter the histamine response. Similar vasodilatory responses to histamine were observed in isolated blood perfused dog and cat kidneys. In contrast, vasoconstrictor responses to histamine occurred in isolated dog and cat kidneys perfused with Krebs' solution and in isolated rabbit kidneys whether perfused with blood or Krebs' solution.

Animals↗
PubMed1976

Modulation and mediation of the action of the renal kallikrein-kinin system by prostaglandins.

The coupling of the kallikrein-kinin and prostaglandin systems within the kidney may be unique: Prostaglandins mediate some of the actions of kinins and modulate others, while depending on the intrarenal generation of kinin to set their level and type of activity. Thus, not only production of prostaglandins but the functional consequences within the kidney of their enhanced production, as determined by the ratio of PGE2 to PGF2alpha, may be subject to regulation by kinins originating intrarenally.

Animals↗
PubMed1975

The actions of bradykinin and eledoisin in the canine isolated kidney: relationships to prostaglandins.

1. The effects of two vasodilator polypeptides, bradykinin and eledoisin, were studied in isolated blood-perfused canine kidneys before and after administration of indomethacin, an inhibitor of prostaglandin synthesis, Bradykinin, but not eledoisin, releases renal prostaglandins. 2. Before administration of indomethacin, bradykinin decreased urinary osmolality and increased free qater clearance, whereas eledoisin did not affect the excretion of solute-free water. After administration of indomethacin, the renal vasodilator action of bradykinin was reduced but the vasodilator action of eledoisin was unaffected. 3. Fractional excretion of sodium was not affected by bradykinin before but was increased after administration of indomethacin. Reduction in glomerular filtration rate contributed to changes in sodium excretion produced by bradykinin and eledoisin. 4. The release of prostaglandins from the kidney by bradykinin amplifies the renal vasodilator action of the kinin and possibly mediates its effect on excretion of solute-free water.

Animals↗
PubMed1971

Intrarenal formation of angiotensin I.

In 5 patients and 16 dogs the mean concentration of angiotensin I, but not II, was higher in the plasma of the renal vein than in the plasma of the renal artery. The fact that I was higher in the vein than in the artery supports the concept that I is formed in the renal vasculature. In the vein the mean concentration of I was 45 times higher than that of II. The probable formation of angiotensin I within the kidney and its high concentration in the renal vein suggest that if the renin angiotensin system plays a role in the regulation of intrarenal blood flow, then angiotensin I may be the major effector hormone in this process.

Angiotensin II↗