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T E Lohmeier

Publications and source records attributed to T E Lohmeier.

At least 19 recordsLinked to original sources
PubMed1996

Role of the renin-angiotensin system in mediating the effects of posture on renal function.

This study was designed to quantitate the influence of the neurohumoral activation associated with orthostatic stress on renal hemodynamics and sodium excretion and, furthermore, to determine the importance of the renin-angiotensin system in mediating these changes in renal function. Seven conscious dogs were studied while lying in the recumbent position and, subsequently, after standing in a supporting sling. Experiments were conducted under control conditions and after plasma angiotensin II (ANG II) concentration was fixed at control levels by chronic infusion of captopril (14 micrograms.kg-1.min-1) and ANG II (0.5 +/- 0.02 ng.kg-1.min-1). During control experiments, 45 min of standing increased plasma renin activity twofold, whereas mean arterial pressure, heart rate, and plasma norepinephrine concentration remained unchanged. During standing, glomerular filtration rate (GFR) and renal plasma flow (RPF) fell to 88 +/- 2 and 77 +/- 3% of recumbent values, respectively, whereas filtration fraction (FF) increased 16 +/- 1%. Additionally, urinary (UNaV) and fractional sodium excretion (FENa) decreased to 27 +/- 6 and 30 +/- 7% of recumbent values, respectively. When plasma ANG II concentration was fixed at control levels during standing, there were no significant changes in GFR, whereas increments in FF and reductions in RPF, UNaV, and FENa were attenuated by 63, 40, 30, and 33%, respectively. These data suggest that, in conscious dogs, standing in a supporting sling causes reflex activation of the sympathetic nervous and renin-angiotensin systems, eliciting reductions in GFR, RPF, and UNaV. Furthermore, ANG II contributes significantly to the effects of passive standing on renal hemodynamics and UNaV.

Angiotensin II↗
PubMed1995

Role of atrial natriuretic peptide in long-term volume homeostasis.

1. Long-term volume homeostasis is linked very closely to long-term arterial pressure control through the renal-body fluid feedback mechanism. A key feature of this control system is the ability of the kidneys to respond to changes in arterial pressure by altering renal excretion of salt and water, often referred to as renal-pressure natriuresis. 2. Quantitative studies indicate that ANP secretion is relatively sensitive to changes in atrial pressure and that the rate of hormonal secretion does not adapt to continuous long-term stimulation. 3. Under normal conditions, the renal-body fluid feedback mechanism for arterial pressure control is very efficient in minimizing changes in body fluid volumes during alterations in sodium intake. Therefore, only small changes in atrial pressure and ANP secretion occur. Alterations in plasma ANP concentration within physiological levels have little effect on renal-pressure natriuresis and, therefore, have little impact on volume homeostasis. 4. When the renal-body fluid feedback mechanism for arterial pressure control is impaired and body fluid volumes are elevated, such as in heart failure, large increases in atrial pressure and ANP secretion occur. The resultant pathophysiological plasma levels of ANP exert sustained natriuretic effects and chronically shift renal-pressure natriuresis to lower arterial pressures. In the absence of this chronic effect of ANP on renal-pressure natriuresis, reduced arterial pressure in compensated heart failure would result in protracted retention of salt and water and additional increments in body fluid volumes.

Animals↗
PubMed1995

Influence of the renal nerves on sodium excretion during progressive reductions in cardiac output.

The purpose of this study was to elucidate the role of the renal nerves in promoting sodium retention during chronic reductions in cardiac output. In five dogs, the left kidney was denervated and the urinary bladder was surgically divided to allow separate 24-h urine collection from the innervated and denervated kidneys. Additionally, progressive reductions in cardiac output were achieved by employing an externally adjustable occluder around the pulmonary artery and by servo-controlling right atrial pressure (control = 0.9 +/- 0.2 mmHg) at 4.7 +/- 0.1, 7.5 +/- 0.1, and 9.8 +/- 0.2 mmHg for 3 days at each level. At the highest level of right atrial pressure, the 24-h values for mean arterial pressure (control = 97 +/- 3 mmHg) and cardiac output (control = 2,434 +/- 177 ml/min) were reduced approximately 25 and 55%, respectively; glomerular filtration rate fell by approximately 35% and renal plasma flow by approximately 65%. However, despite the sodium retention induced by these hemodynamic changes, there were no significant differences in renal hemodynamics or sodium excretion between the two kidneys during pulmonary artery constriction. In contrast, after release of the pulmonary artery occluder on day 9, sodium excretion increased more (approximately 28% during the initial 24 h) in innervated than in denervated kidneys. These results suggest that the renal nerves are relatively unimportant in promoting sodium retention in this model of low cardiac output but contribute significantly to the short-term elimination of sodium after partial restoration of cardiac output and mean arterial pressure.

Animals↗
PubMed1995

Hypertension induced by chronic renal adrenergic stimulation is angiotensin dependent.

We designed these studies to assess the role of the renin-angiotensin system in mediating the hypertensive and renal functional effects of chronic renal adrenergic stimulation. Norepinephrine was infused at 0.1 microgram/kg per minute for 7 days directly into the renal artery of uninephrectomized dogs under control conditions (n = 5) or after plasma angiotensin II (Ang II) concentration was fixed at control levels (n = 5) by chronic intravenous infusion of captopril (14 micrograms/kg per minute) and Ang II (0.58 +/- 0.04 ng/kg per minute). During the first 60 minutes of norepinephrine infusion in control dogs, mean arterial pressure increased 9 +/- 4 mm Hg in association with a twofold to threefold rise in plasma renin activity. Additionally, glomerular filtration rate, renal plasma flow, sodium excretion, and fractional sodium excretion decreased to 70 +/- 5%, 64 +/- 5%, 31 +/- 4%, and 38 +/- 6% of control, respectively, while filtration fraction increased 15 +/- 2%. In contrast to the pronounced short-term effects of norepinephrine on renal function, during chronic norepinephrine infusion, all indexes of renal function returned to control levels. However, elevations in both plasma renin activity and mean arterial pressure were sustained and on day 7 were 2.3 +/- 0.6 ng angiotensin I/mL per hour (control, 0.5 +/- 0.1) and 110 +/- 7 mm Hg (control, 90 +/- 3). In dogs with fixed plasma levels of Ang II, acute and chronic changes in renal function induced by norepinephrine were similar to those in control dogs except that acute reductions in glomerular filtration rate tended to be more severe, and changes in filtration fraction and fractional sodium excretion were either attenuated or abolished. Moreover, in the absence of a rise in plasma Ang II concentration, mean arterial pressure did not change either acutely or chronically during norepinephrine infusion. These findings suggest a critical role for Ang II in mediating the hypertension associated with elevated levels of renal adrenergic stimulation that have little or no long-term effect on renal blood flow.

Angiotensin II↗
PubMed1994

Angiotensin and ANP secretion during chronically controlled increments in atrial pressure.

The primary objective of this study was to determine whether angiotensin II (ANG II) has direct effects on the atrium to chronically stimulate the secretion of atrial natriuretic peptide (ANP) by actions that are independent of its vasoconstrictor and fluid-retaining effects that increase ANP secretion indirectly by raising atrial pressure. In five dogs, right atrial pressure (RAP) was controlled at approximately 5.5 mmHg above control levels for 8 days by employing an externally adjustable occluder around the pulmonary artery and a servo-control system, and plasma levels of ANG II were fixed at either normal (days 1-3 and 7-8) or high (days 4-6) physiological concentrations by chronic infusion of captopril+ANG II. When plasma ANG II was maintained at normal levels during servo-control of RAP, plasma ANP concentration increased five- to sixfold and sodium balance was achieved at a reduced arterial pressure (-14 mmHg). In contrast, despite increased plasma levels of ANP, the high rate of ANG II infusion produced marked sodium retention during the initial 24 h; however, the antinatriuresis was not sustained because the servo-control system partially deflated the pulmonary artery occluder to prevent fluid-induced increments in RAP. Moreover, in the absence of a change in RAP, high plasma levels of ANG II did not influence plasma ANP concentration. These findings indicate that the plasma levels of ANP achieved in heart failure increase renal excretory capability and allow fluid balance to be achieved at a substantial fall in mean arterial pressure as long as there is minimal involvement of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1993

Influence of endogenous angiotensin on the renovascular response to norepinephrine.

The purpose of this study was to elucidate the role of endogenous angiotensin II in mediating the renovascular effects of renal adrenergic stimulation. Six conscious dogs instrumented for monitoring of renal blood flow were subjected to step increases every 10 minutes in the rate of norepinephrine infusion into the renal artery. Under control conditions, infusion of norepinephrine (10-40 ng/min per milliliter per minute of control renal blood flow) increased plasma renin activity and decreased renal blood flow progressively by approximately 10-75%. When increments in angiotensin II during norepinephrine infusion were abolished by fixing plasma levels of angiotensin II at either normal or high concentrations by chronic infusion of captopril plus angiotensin II, renal blood flow responses to adrenergic stimulation were greatly attenuated at rates of norepinephrine infusion that decreased renal blood flow up to approximately 40% under control conditions. Thus, acutely generated angiotensin II appeared to contribute to the renovascular effects of norepinephrine. However, when endogenous levels of angiotensin II were suppressed to low levels by chronic infusion of captopril alone, norepinephrine induced severe renal ischemia at much lower rates of infusion than occurred when the renin-angiotensin system was intact. Since this enhanced sensitivity to norepinephrine did not occur during chronic captopril infusion when angiotensin II was given simultaneously at rates that restored mean arterial pressure to normotensive levels or higher, low arterial pressure during chronic captopril administration may predispose the kidneys to excessive renal vasoconstriction during renal adrenergic stimulation.

Angiotensin II↗
PubMed1991

Hormonal and circulatory responses to chronically controlled increments in right atrial pressure.

To study the time-dependent changes in the secretion of atrial natriuretic peptide (ANP) in response to chronic stimulation by controlled increments in atrial pressure, we developed methodology for precise control of right atrial pressure (RAP) in dogs by employing an externally adjustable occluder around the pulmonary artery and a servo-control system. During 7 days of servo-control of RAP at 6.3 +/- 0.1 mmHg above control levels (1.3 +/- 0.1 mmHg), the 24-h coefficient of variation in RAP was 1/45 the variation that occurred under control conditions. After 30 min of increased RAP, mean arterial pressure (MAP) was reduced from 101 +/- 4 to 84 +/- 3 mmHg in association with increments in plasma renin activity (PRA) from 0.6 +/- 0.1 to 2.5 +/- 0.9 ng angiotensin I (ANG I).ml-1.h-1 and in the plasma concentrations of ANP, arginine vasopressin (AVP), and epinephrine from 93 +/- 18 to 484 +/- 61 pg/ml, from 0.5 +/- 0.1 to 9.2 +/- 2.4 pg/ml, and from 82 +/- 27 to 585 +/- 133 pg/ml, respectively. In comparison, on day 7 of servo-control of RAP, sodium balance was achieved and MAP remained depressed (82 +/- 4 mmHg) along with sustained increments in both plasma ANP concentration (482 +/- 67 pg/ml) and PRA (1.7 +/- 0.6 ng ANG I.ml-1.h-1); on the other hand, the plasma concentrations of AVP and epinephrine returned to control levels. This quantitative study indicates that ANP secretion does not chronically adapt to stimulation by increased atrial pressure and suggests that the plasma levels of ANP achieved in heart failure markedly increase renal excretory capability and allow fluid balance to be achieved at a substantial fall in renal perfusion pressure.

Angiotensin I↗
PubMed1991

Role of angiotensin in ameliorating the renal actions of norepinephrine.

To determine the importance of the arterial pressure effects of angiotensin II (ANG II) on renal function during acute renal adrenergic stimulation, we examined the effects of a 2-h intrarenal arterial infusion of norepinephrine (NE) at 0.1 and 0.25 micrograms.kg-1.min-1 on renal function in five conscious dogs during 1) control conditions, 2) servo-control of renal arterial pressure (RAP) at control levels, and 3) chronic captopril administration. The low rate of NE infusion produced an approximately 20% decrease in glomerular filtration rate (GFR) and renal plasma flow (RPF) and an approximately 8-mmHg increase in RAP in association with an approximately 2.5-fold rise in plasma renin activity (PRA). The high rate of NE infusion produced greater increments in both PRA and RAP and an approximately 50% reduction in GFR and RPF. Neither servo-control of RAP nor captopril administration significantly affected the above renal responses to the low rate of NE infusion. In marked contrast, when increases in RAP (approximately 20 mmHg) were prevented at the high rate of NE infusion by servo-control of RAP, both the PRA and renal responses were enhanced. Furthermore, when RAP was reduced (approximately 25 mmHg) as a result of chronically blocking the renin-angiotensin system with captopril, the renal responses to the high rate of NE infusion were exaggerated even further; in four of five dogs, total renal ischemia occurred in response to NE. These results indicate that ANG II indirectly ameliorates the renal actions of renal adrenergic stimulation by increasing RAP.

Angiotensin II↗
PubMed1991

Preservation of renal function by angiotensin during chronic adrenergic stimulation.

The purpose of the present study was to determine the role of angiotensin II (Ang II) in mediating renal responses to chronic intrarenal norepinephrine infusion. Norepinephrine was continuously infused for 5 days into the renal artery of unilaterally nephrectomized dogs at progressively higher daily infusion rates: 0.05, 0.10, 0.20, 0.30, and 0.40 micrograms/kg/min. In three additional groups of dogs, norepinephrine infusion was repeated during chronic intravenous captopril administration to fix plasma Ang II concentration at 1) low levels (no Ang II infused), 2) high levels in the renal circulation (Ang II infused intrarenally at a rate of 1 ng/kg/min), and 3) high levels in the systemic circulation (Ang II infused intravenously at a rate of 5 ng/kg/min). In the control group of animals with intact renin-angiotensin systems, there were progressive increments in mean arterial pressure (from 96 +/- 4 to 141 +/- 6 mm Hg) and plasma renin activity (from 0.4 +/- 0.1 to 10.9 +/- 4.5 ng angiotensin I/ml/hr) and concomitant reductions in glomerular filtration rate and renal plasma flow to approximately 40% of control during the 5-day norepinephrine infusion period. In marked contrast, when captopril was infused chronically without Ang II, mean arterial pressure was 20-25 mm Hg less than that under control conditions, and the renal hemodynamic effects of norepinephrine were greatly exaggerated; by day 3 of norepinephrine infusion, both glomerular filtration rate (16 +/- 2% of control) and renal plasma flow (12 +/- 4% of control) were considerably lower than values in control animals (86 +/- 4% and 80 +/- 8% of control, respectively). Similarly, when a high level of Ang II was localized in the renal circulation during captopril administration, mean arterial pressure was depressed, and again there were pronounced renal responses to norepinephrine. Conversely, when Ang II was infused intravenously during captopril administration, mean arterial pressure was not reduced, and the glomerular filtration rate and renal plasma flow responses to norepinephrine were similar to those that occurred under control conditions. These findings indicate that the renin-angiotensin system prevents exaggerated renal vascular responses to chronic norepinephrine stimulation by preserving renal perfusion pressure.

Angiotensin II↗
PubMed1990

Chronic effects of a physiological dose of ANP on arterial pressure and renin release.

To determine the long-term effects of a physiological dose of atrial natriuretic peptide (ANP) on renin release, the renin response to reductions in renal arterial pressure (RAP) was studied during 1) control conditions and 2) acute and 3) chronic (5 days) intravenous infusion (5 ng.kg-1.min-1) of alpha-human ANP in conscious dogs maintained on a normal sodium intake. Renal perfusion pressure was servo controlled at reduced levels with an inflatable occluder placed around the abdominal aorta just above the renal arteries. Under control conditions, reducing RAP by 30 and 40 mmHg increased plasma renin activity (PRA) 4- to 5- and 9- to 10-fold, respectively. Acute ANP infusion had no significant effect on either basal levels of PRA or the PRA response to reduced RAP. During chronic ANP infusion there was a two- to threefold increment in plasma ANP concentration and approximately a twofold increase in urinary sodium excretion on day 1; however, there were no significant long-term changes in mean arterial pressure, basal PRA, or the levels of PRA achieved during reductions in RAP. These findings indicate that the changes in plasma ANP concentration that occur under normal physiological conditions do not appreciably alter either basal PRA or renin release in response to renal hypotension in conscious sodium-replete dogs studied under resting conditions.

Animals↗
PubMed1989

Sustained increases in plasma epinephrine concentration do not modulate renin release.

We examined the relationship between plasma renin activity (PRA) and renal arterial pressure (RAP) during 1) control conditions, 2) acute, and 3) chronic intravenous epinephrine (EPI) infusion (125 ng.kg-1.min-1). In eight conscious uninephrectomized dogs maintained on a normal sodium intake, the renin stimulus-response curve (RSRC) was determined by a stepwise reduction in RAP with an inflatable occluder around the renal artery controlled by a servo unit. The RSRC could be approximated by two lines intersecting at a threshold pressure (approximately 20 mmHg below control RAP). In the high-pressure range, PRA was relatively insensitive to changes in RAP, whereas, below threshold pressure, changes in RAP had large effects on PRA. During acute EPI infusion there was approximately a 40% increase in heart rate (control = 57 +/- 3 beats/min) and hematocrit (control = 30 +/- 1%) in association with a rise in plasma EPI concentration from 73 +/- 16 to 1,413 +/- 100 pg/ml; mean arterial pressure (MAP) was unchanged (94 +/- 3 mmHg). Moreover, EPI acutely increased basal PRA from 0.3 +/- 0.1 to 0.8 +/- 0.3 ng angiotensin I.ml-1.h-1 and shifted the RSRC to the right (increasing threshold pressure 7 mmHg) without altering the slope of the RSRC curve either above or below threshold pressure. In contrast, although plasma EPI concentration and hematocrit remained elevated during chronic EPI infusion, heart rate and basal PRA returned to preinfusion values. In addition, there were no significant long-term changes in MAP or in any of the parameters of the RSRC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Chronic hypotensive effects of verapamil in angiotensin hypertension are steroid independent.

This study was designed to examine the mechanisms that contribute to the chronic hypotensive effects of verapamil during angiotensin II-induced hypertension. Hypertension was induced in five dogs by continuous intravenous infusion of angiotensin II (5 ng/kg/min) for 17 days. On the sixth day of angiotensin II infusion when daily sodium balance was achieved, mean arterial pressure (control, 92 +/- 4 mm Hg), plasma aldosterone concentration (control, 5.2 +/- 0.9 ng/dl), and renal resistance (control, 0.28 +/- 0.01 mm Hg/ml/min) were increased 37 +/- 8 mm Hg, 13.6 +/- 5.0 ng/dl, and 0.20 +/- 0.05 mm Hg/ml/min, respectively. At this time there were no significant changes in glomerular filtration rate, effective renal plasma flow, net sodium and water balance, or extracellular fluid volume. Subsequently, when verapamil was infused (at 2 micrograms/kg/min) simultaneously with angiotensin II (days 7-13), there was a net loss of 55 +/- 10 meq sodium, a 7.0 +/- 0.7% fall in extracellular fluid volume, and approximately a 70% reduction in the chronic effects of angiotensin II on mean arterial pressure and renal resistance; in contrast, verapamil failed to attenuate the long-term aldosterone response to angiotensin II. Further, although glomerular filtration rate and effective renal plasma flow tended to increase during verapamil administration, there were no consistent chronic long-term changes in these renal indexes. In comparison with these responses in hypertensive dogs, when verapamil was infused for 7 days before the induction of angiotensin II hypertension, there were no significant changes in any measurements except mean arterial pressure, which fell 11 +/- 1 mm Hg. Thus, these data fail to support the hypothesis that the chronic stimulatory actions of angiotensin II on aldosterone secretion are dependent on a sustained increase in transmembranal calcium influx. Moreover, these data indicate that the pronounced long-term hypotensive effects of verapamil in angiotensin II hypertension are due to impairment of the direct renal actions of angiotensin II rather than the indirect sodium-retaining effects that are mediated via aldosterone secretion.

Aldosterone↗
PubMed1988

Disparity between renal venous norepinephrine and renin responses to sodium depletion.

To evaluate the hypothesis that sodium depletion produces a chronic increase in renal nerve activity, arterial and renal venous plasma norepinephrine (NE) concentrations were measured in conscious dogs subjected to various degrees of sodium depletion. After 9 days of sodium depletion (LS), there was a net loss of 69 +/- 10 meq sodium, and mean arterial pressure (MAP) was reduced from 94 +/- 5 to 88 +/- 4 mmHg. At this time plasma renin activity (PRA) was increased from a control level (sodium intake = 45 meq/day) of 0.34 +/- 0.08 to 1.47 +/- 0.26 ng angiotensin I (ANG I).ml-1.h-1 in association with an approximately sixfold increase in the PRA gradient across the kidneys. Subsequently, when captopril was infused during an additional 7 days of sodium deprivation [(LS + converting enzyme inhibitor CEI)], there was further sodium depletion (31 +/- 11 meq) and hypotension (MAP = 65 +/- 6 mmHg) and PRA and the renal PRA gradient increased even further. In marked contrast, there were no significant changes in either arterial plasma NE concentration (control = 102 +/- 5 pg/ml) or the renal arteriovenous gradient of plasma NE concentration during either LS or LS + CEI. These experiments show a distinct disparity between changes in the PRA and the plasma NE concentration gradient across the kidneys during LS and fail to support the contention that increased renal nerve activity is an important long-term adaptive response to sodium depletion.

Animals↗
PubMed1986

Cardiovascular and renal responses to chronic vasopressin infusion.

Arginine vasopressin (AVP) was infused into the renal artery of seven uninephrectomized conscious dogs at successive rates of 0.09, 0.36, and 1.46 ng X kg-1 X min-1 for 18, 9, and 5 days, respectively; subsequently, the nonpressor analogue of AVP, 1-desamino-8-D-arginine vasopressin (DDAVP), was infused intrarenally for 7 additional days. The lowest infusion rate of AVP produced a high concentration of AVP in the renal circulation (maximal antidiuresis) with only a relatively moderate increase in peripheral plasma AVP concentration. For comparison, the effects of a comparable increase in peripheral plasma AVP concentration during intravenous infusion at this same rate were observed in an additional group of dogs. Acutely, when this low dose of AVP was infused either intrarenally or intravenously, there was marked antidiuresis, but there were no significant changes in mean arterial pressure (MAP), renal hemodynamics, or urinary electrolyte excretion. Chronically, in both groups of animals, cumulative water balance was positive, and glomerular filtration rate, effective renal plasma flow, and MAP (16-18 mmHg) all increased; plasma renin activity decreased. Similar changes were observed during DDAVP infusion. When elevated peripheral plasma levels of AVP were achieved during the higher infusion rates of AVP, natriuresis and diuresis occurred, but, otherwise there was little change in the above variables, including MAP. Thus the hydrosmotic effects of AVP appear to account for its moderate hypertensive activity. Further, the failure of AVP to produce prominent hypertension, even when pronounced systemic vasoconstrictor effects are manifested, may be a result of its inability to promote significant renal vasoconstriction and antinatriuresis.

Aldosterone↗
PubMed1986

Current concepts and perspectives of renal volume regulation in relationship to hypertension.

The renal-body fluid mechanism for arterial pressure control is almost certainly the most primitive of all the pressure-regulating mechanisms in animals. Through the stages of evolution, the system has been greatly improved. Nervous controls provide rapid pressure-control mechanisms that function almost instantaneously, many hours or days before the renal-body fluid mechanism can act fully. The renin-angiotensin-aldosterone system plays another important role: this system ensures that very large changes in salt intake, from as little as one-tenth normal up to as high as 10 times normal, have very little effect on the regulated level of the arterial pressure. Finally, the long-term autoregulatory mechanism helps to dissociate the long-term control of cardiac output from long-term control of arterial pressure; it also makes it possible for extremely slight increases in body fluid volume to cause chronic volume-loading hypertension.

Aldosterone↗
PubMed1981

Blood pressure regulation: basic concepts.

In this paper we have attempted to explain the difference between proportional pressure control systems and the renal-blood volume-pressure control mechanism, which is an infinite gain pressure control system. Because of this infinite gain of the kidney mechanism, this mechanism has the capability of returning arterial pressure all the way back to the control leve. Furthermore, this mechanism can override the other pressure control mechanisms because of its extreme control capability. On the other hand, the renal-blood volume mechanism for pressure control itself be controlled by many other factors. These other factors are said to change the pressure "set-point" level of the renal system, and then the renal system automatically brings the pressure to the set-point level. It is especially noteworthy, however, that some of the factors that play extreme roles in short-term pressure control-such as heart strength, vascular capacity, and total peripheral resistance-will not alter the long-term arterial pressure level (unless they in some way concurrently alter the set-point of the kidney mechanism).

Aldosterone↗
PubMed1980

The role of the renal effects of angiotensin II in hypertension.

The renin-angiotensin system is involved in many forms of clinical and experimental hypertension. Although angiotensin II has powerful vasoconstrictor properties, it is doubtful that any substance can produce sustained hypertension solely by increasing total peripheral resistance. Since the authors have demonstrated previously that alterations in the kidney's ability to excrete sodium can affect long-term arterial blood pressure regulation, they investigated angiotensin's effect on renal function in several experimental models. The results of these studies clearly demonstrate that angiotensin has a powerful direct antinatriuretic effect, the magnitude of which is sufficient to cause marked hypertension at angiotensin concentrations well within the pathophysiological range.

Angiotensin II↗