Mechanisms of escape from sodium retention during angiotensin II hypertension

Hall, John E.; Granger, Joey P.; Hester, Robert L.; Coleman, Thomas G.; Smith, M. J.; Cross, Ron B.

doi:10.1152/ajprenal.1984.246.5.f627

Cited by 64 publications

(83 citation statements)

References 16 publications

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“…The resulting increase in natriuresis establishes a new steady state at increased body Na ϩ and water content at the expense of hypertension suggests an initial failure in balance sensitivity. 11 Other investigators showed earlier that DOCA salt increases blood pressure by increasing sympathetic nerve activity, which should increase the cardiovascular sensitivity to volume. 8 Observations from DOCA salt mice that the blood pressure increase is caused by increased peripheral vascular resistance, rather than increased cardiac output with subsequent readjustments, 12 as well as the finding that venomotor tone is increased in DOCA salt rats, 13 underscore the role of cardiovascular volume sensitivity in DOCA salt hypertension.…”

Section: Titze Et Almentioning

confidence: 95%

Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

et al. 2006

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Abstract-Water-free Na ϩ storage may buffer extracellular volume and mean arterial pressure (MAP) in spite of Na ϩ retention. We studied the relationship among internal Na ϩ , K ϩ , water balance, and MAP in Sprague-Dawley rats, with or without deoxycorticosterone-acetate (DOCA) salt, with or without ovariectomy (OVX). The rats were fed a low-salt (0.1% NaCl) or high-salt (8% NaCl) diet for 5 weeks. DOCA salt increased MAP (161Ϯ14 versus 123Ϯ4 mm Hg; PϽ0.05), and DOCA-OVX salt increased MAP further (181Ϯ22 mm Hg; PϽ0.05). DOCA salt increased the total body Na ϩ by Ϸ40% to 45%; however, water-free Na ϩ retention by osmotically inactive Na ϩ storage and by osmotically neutral Na ϩ /K ϩ exchange allowed the rats to maintain the extracellular volume close to normal. DOCA-OVX salt rats showed similar Na ϩ retention. However, their osmotically inactive Na ϩ storage capacity was greatly reduced and only partially compensated by neutral Na ϩ /K ϩ exchange, resulting in greater volume retention despite similar Na ϩ retention. For every 1% wet weight total body water gain, MAP increased by 2.3Ϯ0.2 mm Hg in DOCA salt rats and 2.5Ϯ0.3 mm Hg in DOCA-OVX salt rats. Because water-free Na ϩ retention buffered total body water content by 8% to 11% wet weight, we conclude that this internal Na ϩ escape buffered MAP. Extrarenal Na ϩ and volume balance seem to play an important role in long-term volume and MAP control. Key Words: electrolytes Ⅲ gender Ⅲ water-electrolyte balance Ⅲ hypertension, sodium-dependent S alt sensitivity describes a reproducible relationship between increasing salt intake and blood pressure. 1 Blood pressure may increase because of increased cardiac output, increased peripheral resistance, or both. Volume-dependent and volume-independent factors contribute. Volumeindependent factors include autonomic nerve activity and molecules that modulate peripheral vascular resistance and heart muscle work. Volume-dependent aspects are based on extracellular fluid volume (ECV). Na ϩ is the major extracellular cation that osmotically acts to hold ECV water; the total body Na ϩ (TBNa ϩ ) has become synonymous for volume regulation. 2,3 Deoxycorticosterone-acetate (DOCA) decreases renal Na ϩ excretion and increases TBNa ϩ and total body volume. DOCA salt is a "prototype" model for salt-sensitive hypertension. 4 Secondary renin-angiotensin-aldosterone system suppression, 5 increased secretion of natriuretic peptides, 6 and altered pressure natriuresis 7 establish a new steady state between Na ϩ intake and Na ϩ excretion at a new blood pressure level. The kidneys escape the mineralocorticoid signal, and additional salt retention ceases, albeit with increased blood pressure. 8 We showed recently that DOCA rats given 1% saline accumulated 4.75 mmol Na ϩ . 9 Only 20% of this Na ϩ load exerted osmotic activity and led to water retention, whereas the rest accumulated as water free by osmotically inactive Na ϩ storage and/or osmotically neutral Na ϩ /K ϩ exchange. In Sprague-Dawley rats, we found that ovariectomy (OVX) reduced th...

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Section: Titze Et Almentioning

confidence: 95%

Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

et al. 2006

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“…Ang II-associated pressure natriuresis appears to serve as a negative feedback system on sodium retention produced by Ang II. The physiological importance of this mechanism is illustrated by the observation that if renal perfusion was prevented from rising by a servo control device during Ang II infusion, renal sodium reabsorption continued to rise to the point of pulmonary edema (40). Even with continued Ang II infusion, release of the renal clamp led to increased urinary sodium excretion with resolution of pulmonary edema (40).…”

Section: Renal Actions Of Angiotensin IImentioning

confidence: 99%

“…The physiological importance of this mechanism is illustrated by the observation that if renal perfusion was prevented from rising by a servo control device during Ang II infusion, renal sodium reabsorption continued to rise to the point of pulmonary edema (40). Even with continued Ang II infusion, release of the renal clamp led to increased urinary sodium excretion with resolution of pulmonary edema (40). Thus, the net effect of different levels of Ang II on sodium and water excretion depends critically on the balance between the antinatriuretic actions of Ang II and the effect of increased renal perfusion pressure that tends to cause natriuresis.…”

Section: Renal Actions Of Angiotensin IImentioning

confidence: 99%

Renal actions of angiotensin-(1-7)

Silva¹,

Baracho²,

Passaglio³

et al. 1997

Braz J Med Biol Res

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The heptapeptide angiotensin-(1-7) is considered to be a biologically active endproduct of the renin-angiotensin system. This angiotensin, which is devoid of the most known actions of angiotensin II such as induction of drinking behavior and vasoconstriction, has several selective effects in the brain and periphery. In the present article we briefly review recent evidence for a physiological role of angiotensin-(1-7) in the control of hydroelectrolyte balance.

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“…For example, an increase in renal perfusion pressure was essential in offsetting the sodium-retaining actions of long-term infusions of aldosterone or angiotensin II. 20 - 21 When renal perfusion pressure was prevented from increasing as hypertension developed, sodium retention continued, and in some experiments the extracellular fluid volume expansion that occurred resulted in severe circulatory disturbances such as pulmonary edema, ascites, or both. However, these studies did not quantitate the importance of renal perfusion pressure per se on renal function.…”

Section: Discussionmentioning

confidence: 99%

Role of pressure natriuresis in long-term control of renal electrolyte excretion.

et al. 1993

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If pressure natriuresis is to play an important role in arterial pressure control, renal perfusion pressure must have a long-term effect on urinary sodium excretion. The aim of this study was to quantitate the importance of renal perfusion pressure per se in controlling renal hemodynamics and electrolyte excretion chronically. Female mongrel dogs (n=6) were instrumented with bilateral renal artery catheters for measurement of renal perfusion pressure and occluders on both renal arteries for servo-control of renal perfusion pressure at different levels; the urinary bladder was split for determination of renal clearances and electrolyte excretion from each kidney separately. Because both kidneys were exposed to the same neurohumoral influences, any changes in renal function could be attributed to differences in renal perfusion pressure between the two kidneys. After 5 days of control, renal perfusion pressure to one kidney was reduced from 86.7 ±0.2 to 74.2 ±0.6 mm Hg for 12 days, and pressure in the contralateral kidney increased to 91.5±0.4 mm Hg. Sodium excretion decreased from 41±2 to 25±1 mmol/d in the servo-controlled kidney and increased from 41 ±1 to 55 ±1 mmol/d in the contralateral kidney during 12 days of servo-control. Urine volume, chloride excretion, and potassium excretion exhibited similar patterns during servo-control. In addition, autoregulation of effective renal plasma flow and glomerular filtration rate was relatively well maintained; however, in the low-pressure kidney, glomerular filtration rate was slightly but significantly lower (-8%) than in the contralateral kidney. In summary, long-term changes in renal perfusion pressure caused sustained alterations in renal electrolyte excretion. These results suggest that renal perfusion pressure is an important long-term controller of sodium and water excretion. over the long-term by complex interactions J~ A . between the various neurohumoral control systems and the ability of the kidneys to excrete salt and water. Guyton and colleagues 1 (see References 2 through 5 for review) have emphasized renal-body fluid feedback as the dominant control system for long-term blood pressure control. A key component of this feedback is the effect of arterial pressure on renal excretion of sodium, often referred to as pressure natriuresis. In most instances, this mechanism is believed to stabilize blood pressure in response to various perturbations that would tend to cause hypertension or hypotension.The validity of this concept depends on the assumption that arterial pressure has a long-term influence on renal excretion of sodium and water, a premise that has been difficult to test experimentally. Numerous investigators have demonstrated that acute changes in arterial pressure markedly alter sodium and water excretion, 69 but the long-term effects of pressure per se on renal excretion are largely unknown. Long-term pressurenatriuresis curves are usually determined indirectly by

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Mechanisms of escape from sodium retention during angiotensin II hypertension

Cited by 64 publications

References 16 publications

Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

Renal actions of angiotensin-(1-7)

Role of pressure natriuresis in long-term control of renal electrolyte excretion.

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Mechanisms of escape from sodium retention during angiotensin II hypertension

Cited by 64 publications

References 16 publications

Extrarenal Na + Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

Extrarenal Na + Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

Renal actions of angiotensin-(1-7)

Role of pressure natriuresis in long-term control of renal electrolyte excretion.

Contact Info

Product

Resources

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Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats