Hemodynamic responses to acute volume expansion in Dahl salt-sensitive rats

Reddy, Ramasubba; Baylis, Chris

doi:10.1152/ajpregu.1991.260.1.r32

Cited by 6 publications

(10 citation statements)

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“…In calculating SVR, other investigators have also made the tacit assumption that CVP or right atrial pressure does not change with NaCl loading. 16 -18 Yet, in Dahl SS but not in Dahl SR rats, right atrial pressure increased slightly but significantly by 2.8 mm Hg when NaCl intake was increased 16-fold for 5 days and by 1.5 mm Hg when it was increased 7-fold, 26 as in the current study. Such a small NaCl-induced increase of CVP in SS subjects but not in SR subjects would have resulted in smaller NaClinduced group differences in SVR than those reported.…”

Section: Limitationssupporting

confidence: 65%

What Initiates the Pressor Effect of Salt in Salt-Sensitive Humans?

2007

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Abstract-We tested the traditional hypothesis that an abnormally enhanced renal reclamation of dietary NaCl alone initiates its pressor effect ("salt sensitivity"). Under metabolically controlled conditions, we grouped 23 normotensive blacks as either salt-sensitive (SS) or salt-resistant (SR), depending on whether or not dietary NaCl loading did or did not increase mean arterial blood pressure (MAP) by Ն5 mm Hg. We determined whether dietary NaCl loading induces greater increases in external Na ϩ balance, plasma volume, and cardiac output in SS, compared with any in SR subjects, and differential changes in systemic vascular resistance (SVR) that could account for the pressor differences between SS and SR subjects. Using impedance cardiography, we measured cardiac output and SVR daily at 4-hour intervals throughout the last 3 days of a 7-day period of low NaCl intake (30 mmol per day) and throughout a subsequent 7-day period of NaCl loading (250 mmol per day). In the 11 SS subjects, compared with the 12 SR subjects, NaCl loading induced no greater increases in Na ϩ balance, body weight, plasma volume, and cardiac output. Yet, from days 2 to 7 of NaCl loading, changes of MAP in SS diverged progressively from those in SR. From days 2 to 4, progressive increases of MAP in SS subjects reflected importantly impaired decreases of SVR, as judged from "normal" decreases of SVR in SR subjects. In SS and SR subjects combined, changes in both MAP and SVR on day 2 strongly predicted changes in MAP on day 7. In many normotensive blacks, vascular dysfunction is critical to the initiation of a pressor response to dietary NaCl. Key Words: blood pressure Ⅲ sodium chloride Ⅲ electrolyte balance Ⅲ vascular resistance Ⅲ cardiac output S alt sensitivity, blood pressure (BP) that varies directly with dietary NaCl, characterizes much of human "essential" hypertension and increases the likelihood of the occurrence of hypertension, cardiovascular disease, and death. 1-3 It is widely formulated that dietary NaCl induces a persisting pressor effect only by an abnormal enhancement of its renal reclamation that entrains over days this physiological sequence: positive Na ϩ balance, plasma volume expansion, a transient increase in cardiac output (CO), and a sustained increase in systemic vascular resistance (SVR). As formulated, the increase in CO peaks during the initial 3-to 4-day period of NaCl loading, when it alone elicits the initial pressor effect of NaCl and SVR remains "normal." The pressor effect is sustained by the increase in SVR, which occurs in normal autoregulatory response to the increase in CO. 4 -6 Although the restrictively renal dysfunction formulated accords with many observations, 7,8 recent observations in animal models of genetically determined salt-sensitive hypertension accord with the formulation that dietary NaCl loading can induce a pressor effect that depends on a dysfunctional vascular response to dietary NaCl. 9,10 Neither formulation has been tested rigorously in humans. That would require examining the effec...

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Section: Limitationssupporting

confidence: 65%

What Initiates the Pressor Effect of Salt in Salt-Sensitive Humans?

2007

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“…As we have previously described 18 for measurement of cardiac output, the left carotid artery was catheterized with a thermistor-catheter combination. The right jugular vein was catheterized with Tygon microbore tubing (0.015 inch i.d.xO.030 inch o.d.…”

Section: Methodsmentioning

confidence: 99%

Dietary sodium chloride increases blood pressure in obese Zucker rats.

Reddy

1992

Hypertension

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In the rat, elevated arterial pressure is not consistently associated with obesity. The purpose of this study was to compare measurements of blood pressure, cardiac output, and total peripheral resistance in obese and lean Zucker rats on different NaCI intakes. Obese and lean rats drank either water or isotonic NaCl for 18 days. Tail systolic blood pressures of saline-drinking obese rats were higher than all other groups (p<0.05). NaCl intake did not affect blood pressure in lean rats, and blood pressures of water-drinking obese rats did not differ from those of lean controls. In a subsequent experiment, direct arterial pressures and cardiac outputs (thermodilution) were measured in separate groups of conscious rats that had been maintained on a 1% or 4% NaCl intake for 12 weeks. Arterial pressure was higher (p<0.01) in obese rats fed 4% NaCl (130±4 mm Hg) than in obese rats fed 1% NaCl (118±2 mm Hg) or than in lean rats fed either NaCl intake (118±3 mm Hg and 116±3 mm Hg, respectively). Cardiac output of obese rats was higher than that of lean rats (/xO.Ol); however, the NaCl-induced increase of blood pressure was accounted for by an increase of peripheral resistance (p<0.01). Thus, in contrast to the lean Zucker rat, arterial pressure of the obese Zucker rat is increased by a high dietary intake of NaCl. Obesity-related hypertension has been ascribed to hypervolemia and an increased cardiac output without an appropriate reduction of peripheral resistance 2 and to increased sympathetic nervous system activity.3 Further, it has been suggested that insulin resistance associated with obesity contributes to hypertension. 4 The Zucker fatty rat inherits obesity as an autosomal recessive trait.3 Rats homozygous for the fatty gene are also insulin resistant and hyperinsulinemic. Based on indirect, tail-cuff measurements and direct measurement of intra-arterial pressure, several reports have indicated that blood pressure of the obese Zucker rat does not differ from that of lean controls.6 -10 In contrast, other reports have indicated that arterial pressure is increased in this animal model. 11 -15 One purpose of the present study was to compare measurements of arterial pressure, cardiac output, and peripheral resistance in obese Zucker rats and lean controls.In the human, there is some evidence that obesityrelated hypertension is salt sensitive.16 ' 17 Consequently, we hypothesized that blood pressure in this rat model of obesity would be increased by a high NaCl intake. In the present study, arterial pressures were compared in obese and lean Zucker rats on normal and high NaCl intakes. MethodsIn protocol 1, we evaluated the effect of a high NaCl intake in obese and lean rats by measuring indirect blood pressures in the tail. In protocol 2, direct arterial pressures and cardiac outputs were measured in separate groups of chronically instrumented, conscious obese and lean rats fed either a normal or a high NaCl diet.For both protocols, lean and obese female Zucker rats were purchased from Harlan Sprague Dawley, Inc., ...

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“…4,18 We demonstrated previously 4 that in Dahl S rats the impairment of arterial baroreflex control of RSNA and HR by high salt intake can be prevented by blockade of brain "ouabain." The present study confirms this previous finding and demonstrates that in Dahl S rats blockade of brain "ouabain" also prevents the impairment of cardiopulmonary baroreflex control of RSNA and HR by high salt intake.…”

Section: Brain Ang II and Impairment Of Baroreflex Functionmentioning

confidence: 96%

Both Brain Angiotensin II and “Ouabain” Contribute to Sympathoexcitation and Hypertension in Dahl S Rats on High Salt Intake

1998

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Abstract-Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats from 5 to 9 weeks of age received a regular or high salt diet and concomitantly an intracerebroventricular infusion of the angiotensin type 1 blocker losartan (1 mg ⅐ kg Ϫ1 ⅐ d Ϫ1) or antibody Fab fragments, which bind ouabain and related steroids with high affinity, or ␥-globulins as control (200 g/d for both). At 9 weeks of age, blood pressure (BP), heart rate (HR), central venous pressure, and renal sympathetic nerve activity were recorded in conscious rats at rest and in response to air stress and to intracerebroventricular ␣ 2 -agonist guanabenz (50 g) and ouabain (0.5 g). Baroreflex function was assessed by acute volume expansion with intravenous 5% dextrose and ramp changes of BP by Ϯ50 mm Hg induced by intravenous phenylephrine and sodium nitroprusside. In Dahl S but not R rats, high salt significantly increased BP and HR; enhanced BP, HR, and renal sympathetic nerve activity responses to air stress and guanabenz; and attenuated cardiopulmonary and arterial baroreflex control of renal sympathetic nerve activity and HR. Both losartan and Fab fragments prevented these responses to high salt to a similar extent in Dahl S rats but had no effect in Dahl R rats on high salt. Sympathoexcitatory responses to ouabain were attenuated in Dahl S on high versus regular salt and were abolished in Dahl R or S treated with losartan or Fab fragments. Consistent with previous studies in SHR, the present data indicate that in Dahl S on high salt, both brain "ouabain" and angiotensin II contribute to decreased sympathoinhibition and increased sympathoexcitation, impairment of baroreflex, and therefore hypertension. (Hypertension. 1998;32:1028-1033.) Key Words: sympathetic nervous system Ⅲ baroreflex Ⅲ losartan Ⅲ stress Ⅲ guanabenz Ⅲ antibody Fab fragments N eural mechanisms leading to sympathetic hyperactivity play a major role in the pathogenesis of salt-dependent hypertension in Dahl salt-sensitive (Dahl S) rats.1 In Dahl S rats, high salt intake enhances sympathoexcitatory responses and attenuates sympathoinhibitory responses.2 Arterial 3,4 and cardiopulmonary 5 baroreflex control of efferent sympathetic nerve activity and/or heart rate (HR) are impaired in Dahl S rats, even before the commencement of high salt intake. 3,5 High salt intake also causes sympathetic hyperactivity 6 and impairment of baroreflex function 7 in spontaneously hypertensive rats (SHR), another model of salt-sensitive hypertension. In a series of studies we have shown that high salt intake increases ouabain-like activity ("ouabain") 8,9 in several brain areas and that in both SHR and Dahl S rats, blockade of brain "ouabain" prevents sympathoexcitation, baroreflex impairment, and exaggeration of hypertension. 2,4,6,9 In SHR, it appears that high dietary salt increases brain "ouabain" and the latter exerts its sympathoexcitatory and pressor effects via the brain renin-angiotensin system (RAS).6 Whether brain angiotensin II (Ang II) is also involved in the impairment of baroreflex ...

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Hemodynamic responses to acute volume expansion in Dahl salt-sensitive rats

Cited by 6 publications

References 0 publications

What Initiates the Pressor Effect of Salt in Salt-Sensitive Humans?

What Initiates the Pressor Effect of Salt in Salt-Sensitive Humans?

Dietary sodium chloride increases blood pressure in obese Zucker rats.

Both Brain Angiotensin II and “Ouabain” Contribute to Sympathoexcitation and Hypertension in Dahl S Rats on High Salt Intake

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