Renal blood flow and its response to angiotensin II. An interaction between oral contraceptive agents, sodium intake, and the renin-angiotensin system in healthy young women.

Hollenberg, Norman K.; Williams, Gordon H.; Burger, Bruno; Chenitz, W; Hoosmand, I; Adams, Douglass F.

doi:10.1161/01.res.38.1.35

Cited by 68 publications

(45 citation statements)

References 54 publications

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“…The renal vascular reactivity to norepinephrine was not significantly influenced by alteration of sodium balance or by administration of converting enzyme (except for an enhancement of norepinephrine sensitivity which occurred after CEI in dogs pretreated with DOCA and salt). All to normal women receiving estrogein-containing oral contraceptives (52). Similarly, it may explain the blunted pressor sensitivity to All in a variety of diseases (7,9,(14)(15)(16)(17).…”

Section: Resultsmentioning

confidence: 97%

The effect of altered sodium balance upon renal vascular reactivity to angiotensin II and norepinephrine in the dog. Mechanism of variation in angiotensin responses.

Oliver¹,

Cannon²

1978

J. Clin. Invest.

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A B S T R A C T The mechanism whereby the vasoconstrictor response to angiotensin II (A,,) is influenced by sodium balance or disease is unclear. To explore this question, the renal vascular responses (RVR) to intrarenal injections of subpressor doses of A,, and norepinephrine were studied in dogs with an electromagnetic flowmeter. Acute and chronic sodium depletion increased plasma renin activity (PRA) and blunted the RVR to A,,, while acute sodium repletion and chronic sodium excess plus desoxycorticosterone acetate decreased PRA and enhanced the RVR to All.The magnitude of the RVR to Al1 was inversely related to PRA. The RVR to norepinephrine was unaffected by sodium balance and was not related to PRA. Inhibition of the conversion of angiotensin I to Al, by SQ 20,881 during sodium depletion lowered mean arterial blood pressure (MABP), increased renal blood flow (RBF), and enhanced the RVR to Al, but not to norepinephrine. Administration of bradykinin to chronically sodium-depleted dogs also lowered the MABP and increased RBF but had no effect on the RVR to A11. SQ 20,881 had no effect on MABP, RBF, or the RVR to Al1 in the dogs with chronic sodiuni excess and desoxycorticosterone acetate. Administration of indomethacin to chronically sodium-depleted dogs lowered RBF but did not influence the RVR to A,,.The results indicate that the RVR to A,, is selectively influenced by sodium balance and that the magnitude of the response is inversely related to the availability of endogenous AII The data did not suggest that the variations in the RVR to A,, were because of direct effects of sodium on vascular contraction, changes in

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Section: Resultsmentioning

confidence: 97%

The effect of altered sodium balance upon renal vascular reactivity to angiotensin II and norepinephrine in the dog. Mechanism of variation in angiotensin responses.

Oliver¹,

Cannon²

1978

J. Clin. Invest.

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“…This is the expected result in patients with high PRA levels because the prolonged presence of high serum AII concentrations has been shown to induce a relative vascular resistance to All. For example, the pressor response to All is blunted in malignant hypertension (13), in cirrhosis (13,15), in sodiumrestricted normal subjects (16), and in women taking oral contraceptives (17), conditions that are all associated with elevated renin and All levels. Thus, because the HREH patients with normal APA:APRA ratios had renin levels higher than sodium-restricted normal subjects, a reduced vascular sensitivity to infused All would be anticipated.…”

Section: Resultsmentioning

confidence: 99%

Abnormal Adrenal Responsiveness and Angiotensin II Dependency in High Renin Essential Hypertension

Dluhy¹,

Bavli²,

Leung³

et al. 1979

J. Clin. Invest.

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A B S T R A C T Adrenal responsiveness to angiotensin II (AII) and the diastolic blood pressure responses to saralasin were studied in 19 patients with high renin essential hypertension (HREH) on a 10-meq Na+/100 meq K+ diet. The increment in plasma renin activity (PRA) between supine and upright positions was used as an estimate of the acute stimulation of the adrenal gland by endogenous AII; the normal increment in plasma aldosterone divided by the increment in PRA was >3.8. 7 of 19 had abnormal upright posture responses with significantly greater mean PRA increments (24+6 ng/ml per h) and significantly smaller plasma aldosterone increments 47±16 ng/dl) (P < 0.036) compared to the increments observed in HREH patients with normal adrenal responsiveness (PRA = 15+1 nglml per h; plasma aldosterone = 87+17 ng/dl). When AII was infused at doses of0.1-3 nglkg per min, only patients with normal posture responses had normal plasma aldosterone increments; plasma aldosterone levels failed to significantly increase even at the highest infusion rate in the patients with the abnormal upright posture responses. The AII competitive inhibitor, saralasin (0.3-30 ,ug/kg per min) was then infused to study the occurrence of angiotensinogenic hypertension in both HREH subgroups. The mean decline in diastolic blood pressure to saralasin in the subnormal adrenal responsive patients (-15±3 mm Hg) was significantly greater than in the normal adrenal responsive group (-3±2 mm Hg) (P < 0.02).It is concluded that patients with HREH are not a homogeneous population; approximately one-third have AII-dependent hypertension. In these patients, the mechanism responsible for the elevated renin and blood pressure could be a compensatory increase Address reprint requests to Dr. Dluhy.

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“…The first-generation OC has been associated with biopsy-proven renal damage in the absence of primary renal disease (35), and healthy women ingesting the high-estrogen OC demonstrated decreased renal blood flow and a blunted response to Ang II (10). In contrast, an increased renal hemodynamic response to Ang II in healthy OC users compared with nonusers was described more recently.…”

Section: ϫ2mentioning

confidence: 99%

“…Ingestion of the oral contraceptive (OC) results in elevated circulating RAS components (10 -12). This laboratory reported reduced renal blood flow and a blunted renal hemodynamic response to Ang II in healthy women using highestrogen dose OCs (10). Ingestion of lowestrogen dose OCs also results in RAS activation with respect to the kidney (11,12).…”

mentioning

confidence: 92%

Oral Contraceptives, Angiotensin-Dependent Renal Vasoconstriction, and Risk of Diabetic Nephropathy

et al. 2005

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OBJECTIVE -Diabetes, the leading cause of end-stage renal disease in the U.S., is believed to involve activation of the renin angiotensin system (RAS) as a risk factor for nephropathy. RAS activation occurs in healthy women using oral contraceptives (OCs), but the effects of OC use on the diabetic kidney are unclear.RESEARCH DESIGN AND METHODS -Renal plasma flow (RPF) response to captopril, as an index of RAS activity, was investigated in 92 women (41 nondiabetic OC nonusers, 10 nondiabetic OC users, 29 diabetic OC nonusers, and 12 diabetic OC users). Based on the hemodynamic findings, we examined the impact of OC use on the development of nephropathy as a post hoc analysis in an inception cohort of 114 female patients with newly diagnosed type 1 diabetes followed for a median of 20.7 years (range 1-24).RESULTS -Nondiabetic OC nonusers showed minimal RPF vasodilator response to captopril (9 Ϯ 10 ml ⅐ min Ϫ1 ⅐ 1.73 m Ϫ2 , P ϭ 0.6). In comparison, nondiabetic OC users showed a significant increase (69 Ϯ 35 ml ⅐ min Ϫ1 ⅐ 1.73 m Ϫ2 , P ϭ 0.02) (P ϭ 0.04 vs. nondiabetic OC nonusers). Diabetic OC nonusers demonstrated the anticipated vasodilator response (58 Ϯ 12 ml ⅐ min Ϫ1 ⅐ 1.73 m Ϫ2 , P Ͻ 0.0001). Diabetic OC users showed the largest responses (84 Ϯ 12 ml ⅐ min Ϫ1 ⅐ 1.73 m Ϫ2 , P ϭ 0.002) (P ϭ 0.04 vs. diabetic OC nonusers). Plasma renin activity did not vary with OC use (P ϭ 0.3). The RPF responses to captopril and angiotensin receptor blocker were highly correlated (r ϭ 0.72, P Ͻ 0.001), suggesting clear involvement of the RAS. In the observational study, 18% (6/33 [95% CI 4.3-32.1]) of OC users developed macroalbuminuria compared with 2% (2/81 [0 -5.9]) of OC nonusers (P ϭ 0.003, univariate analysis). After adjustment for known risk factors with a Cox regression model, OC use remained a predictor for the development of macroalbuminuria (relative risk 8.90 , P ϭ 0.008).CONCLUSIONS -The strong association of OC use with angiotensin-dependent control of the renal circulation and the development of macroalbuminuria suggest that OC use may be a risk factor for diabetic nephropathy. Large prospective studies are required to further investigate this relationship. 28:1988 -1994, 2005 D iabetes is the leading cause of endstage renal disease in the U.S. Moreover, the number of patients diagnosed each year with end-stage renal disease secondary to diabetes is expected to grow from 41,000 in the year 2000 to 300,000 in the year 2030 (1). Activation of the renin angiotensin system (RAS) is associated with progression of both diabetic and nondiabetic kidney disease (2). Numerous studies have demonstrated that RAS blockade lowers the rate of urinary albumin excretion (UAE) and retards decline of renal function in diabetes (3-7). This protective effect probably reflects both the hemodynamic and nonhemodynamic effects of ACE inhibitors and angiotensin II (Ang II) receptor blockers. Diabetes CareFemale sex is a protective factor in the development of renal disease (8), but the mechanism remains elusive. Estrogen plays a role ...

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Renal blood flow and its response to angiotensin II. An interaction between oral contraceptive agents, sodium intake, and the renin-angiotensin system in healthy young women.

Cited by 68 publications

References 54 publications

The effect of altered sodium balance upon renal vascular reactivity to angiotensin II and norepinephrine in the dog. Mechanism of variation in angiotensin responses.

The effect of altered sodium balance upon renal vascular reactivity to angiotensin II and norepinephrine in the dog. Mechanism of variation in angiotensin responses.

Abnormal Adrenal Responsiveness and Angiotensin II Dependency in High Renin Essential Hypertension

Oral Contraceptives, Angiotensin-Dependent Renal Vasoconstriction, and Risk of Diabetic Nephropathy

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