Effects of Aldosterone on Blood Pressure, Water, and Electrolytes

Gross, F.

doi:10.1007/978-3-642-65600-2_19

Cited by 4 publications

(4 citation statements)

References 176 publications

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“…8 Similarly, human subjects treated with doses of aldosterone which produce strong electrolyte effects have either developed mild hypertension or remained normotensive.…”

Section: Discussionmentioning

confidence: 99%

“…7 including isolated membranes from rat kidney, 8 and indirect evidence suggests that adenosine may play a role in the regulation of renal blood flow. For example, in heart and skeletal muscle, adenine nucleotides and adenosine produce vasodilation; 2 ' 4 however, in the dog kidney, ATP and ADP elicit vasodilation, whereas AMP and adenosine elicit vasoconstriction.…”

Section: Adenosine Production In the Ischemic Kidneymentioning

confidence: 99%

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Failure of chronic aldosterone infusion to increase arterial pressure in dogs with angiotensin-induced hypertension.

Lohmeier¹,

Cowley²,

DeClue³

et al. 1978

Circulation Research

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SUMMARY To generate quantitative data relating to the hypertensive activity of aldosterone, 9 /xg/kg per day (4 times normal) aldosterone (4-ALDO) were infused chronically in both adrenalectomized and intact dogs until steady state conditions were achieved. Mean arterial pressure (MAP) was monitored continuously, 24 hours per day, and daily steady state values for MAP based on approximately 600 sample points per day were determined by employing computerized data analysis. In some studies, angiotensin II (A II) was also infused chronically (5 ng/kg per min) prior to and during 4-ALDO administration to maintain plasma levels of A II constant. 4-ALDO infusion in intact dogs maintained on 75 mEq sodium per day increased MAP by only 13 mm Hg compared to a greater than 30 mm Hg rise observed with A II infusion alone, even though plasma aldosterone concentration rose in these experiments only two-thirds as much as when 4-ALDO was infused. When A II was infused chronically, a fall in plasma A II concentration could not compensate for the hypertensive effects of superimposed 4-ALDO infusion; therefore, maximal aldosterone-induced hypertension was expected. However, in both adrenalectomized and intact dogs, the further addition of 4-ALDO failed to increase the degree of A II-induced hypertension and failed to promote sodium retention. Chronic A II infusion in intact dogs maintained on 75 and 190 mEq sodium per day produced a sustained increase in plasma aldosterone concentration (2.7 and 1.6 times control, respectively) as well as kaliuresis and hypokalemia. Infusion of A II in adrenalectomized dogs produced hyperkalemia, not hypokalemia. The data indicate that high plasma levels of aldosterone, at least over a period of several weeks, have only weak hypertensive effects in the dog, particularly in instances in which the aldosteronism is associated with a primary increase in A II.ALTHOUGH aldosterone is considered by many to have an important role in the genesis and maintenance of hypertension associated with increased activity of the renin-angiotensin-aldosterone system, in fact, there are few quantitative data to distinguish the suspected hypertensive effects of the aldosterone from that of simultaneously formed angiotensin. The best example of the blood pressure-elevating effect of aldosterone is the syndrome of primary aldosteronism. Patients with this syndrome have hyperaldosteronemia and mild-to-severe hypertension.

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“…8 Similarly, human subjects treated with doses of aldosterone which produce strong electrolyte effects have either developed mild hypertension or remained normotensive.…”

Section: Discussionmentioning

confidence: 99%

Section: Adenosine Production In the Ischemic Kidneymentioning

confidence: 99%

Failure of chronic aldosterone infusion to increase arterial pressure in dogs with angiotensin-induced hypertension.

Lohmeier¹,

Cowley²,

DeClue³

et al. 1978

Circulation Research

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“…If this increase in uterine receptor concentration is in agreement with the enhanced sensitivity of smooth muscle to angiotensin after sodium loading, the reduction in the steroidogenic effect of angiotensin I1 observed in the same conditions cannot be similarly related to changes at the receptor level and stems probably from a cellular mechanism distal to receptor sites. The potential effect of sodium loading on angiotensin I1 adrenal receptor sites is, however, demonstrated in deoxycorticosterone acetate hypertension and one kidney Goldblatt hypertension, conditions characterized both by a decrease in angiotensin I1 binding capacity and a markedly positive sodium balance (for review see Gross, 1974;Carretero & Romero, 1977).…”

Section: Discussionmentioning

confidence: 99%

Alterations of Adrenal and Uterine Angiotensin II Receptors during Variation of Sodium Intake and/or Experimental Hypertension

et al. 1978

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1. Angiotensin I1 receptors from rat adrenal gland and myometrium were studied during variation of sodium intake.2. In both target-tissues low Na+ diet increased the number of receptors whereas a high Na+ diet did not modify the adrenocortical receptors but increased the number of uterine receptors.3. Deoxycorticosterone and one kidney Goldblatt hypertension were associated with a decrease in the number of adrenal receptors.4. Alterations of angiotensin I1 receptors alone cannot explain satisfactorily the variations of sensitivity of target-cells to angiotensin I1 during sodium balance changes.

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“…After Doca-treatment the renin secretion in the kidney and the formation of angiotensin are strongly suppressed (7). The smaller changes of APA activities that are evident in Doca-treated animals after furosemide seem to be a n expression of the suppressed renin and angiotensin production.…”

Section: Literature Citedmentioning

confidence: 85%

Quantitative histochemistry of the angiotensinase A (APA) in the renal glomeruli of rats after stimulation of the renin‐angiotensin system,

Kügler

Schiebler

1984

Cytometry

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Quantitative histochemical measurements is concluded that glomerular M A activities of aminopeptidase A ( M A , angiotensinase A) correspond to the reninlangiotensin plasma were done kinetically in the kidney glomeruli levels and that the fast changes of APA activof rats after short-term experiments (treat-ities are well demonstrable by kinetic densiment with furosemide as well as captopril for tometric measurements in situ. 2, 4, and 6 h). The APA activities increased after treatment with furosemide or captopril.Highest activities were determined after 4 h using furosemide and 6 h using captopril. I t Key terms: Quantitative histochemistry, aminopeptidase A, kidney glomeruli Microdensitometric (microphotometric) procedures make it possible to determine enzyme activities in tissue sections at cellular level (1,2,4,8,9,11,20,24). The combination of microdensitometers (microphotometers) with computers allows kinetic determinations of enzyme activities in tissue sections, and therefore maximal enzyme activities now can be recorded in the range of linear kinetics (11,22,23).The application of such quantifying procedures on proteinase histochemistry in the kidney (8,(13)(14)(15) has shown that a special aminopeptidase in the glomerulus and the brush border of the proximal tubule, namely the membrane-bound aminopeptidase A (APA; 12, 17), is the socalled angiotensinase A (13~5). This peptidase cleaves N-terminal aspartic acid from angiotensin I and I1 (ANG I, II) and is to be considered as a component of the reninangiotensin system (RAS) in the kidney.In the present quantitative histochemical study we used short-term experiments in rats with furosemide and captopril, which stimulate the RAS in different ways (6,10), to show that glomerular APA activities change rapidly in accordance with the condition of the RAS. It is possible to record early changes in a hormonal system using quantitative histochemistry. MATERIALS AND METHODS Animal MaterialThe investigations were performed in a total of 70 adult male Wistar rats of our own breeding. Before the experiments (see below) the animals were selected according to bodyweight (BW, 285-310 g) and age (75 to 95 cl). The animals were housed in Makrolori cages at 21 2°C with light-dark changes a t 12-h intervals. Tap water and standard altromin feed (TPF 1320) were given ad libitum.For the experiments the animals were divided into five groups: Group I consisted of 15 rats that received a single intraperitoneal (i.p.) injection of 10 mg/100 g BW furosemide (LasixR, 250 mg from Hoechst). Five rats each were killed 2,4, and 6 h after the beginning of the treatment. Group I1 consisted of 15 rats that received a single i.p. injection of 0.1 mg/100 g BW captopril(O.3 mg dissolved in 1 ml 0.85% NaCl solution; captopril was a gift of von Heyden company). Five rats each were killed 2,4, and 6 h after the beginning of the treatment. Group I11 (controls for group I and 11) consisted of 15 rats that received a single i.p. injection of 0.33 mVlOO g BW 0.85% NaCl solution. Five rats each were ...

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Effects of Aldosterone on Blood Pressure, Water, and Electrolytes

Cited by 4 publications

References 176 publications

Failure of chronic aldosterone infusion to increase arterial pressure in dogs with angiotensin-induced hypertension.

Failure of chronic aldosterone infusion to increase arterial pressure in dogs with angiotensin-induced hypertension.

Alterations of Adrenal and Uterine Angiotensin II Receptors during Variation of Sodium Intake and/or Experimental Hypertension

Quantitative histochemistry of the angiotensinase A (APA) in the renal glomeruli of rats after stimulation of the renin‐angiotensin system,

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