Left ventricular hypertrophy (LVH), a target organ response in essential hypertension, is only weakly related to clinical measurements of blood pressure. To determine whether blood pressure measured under basal or stress conditions more closely determines LVH, we compared echocardiographic left ventricular mass index and relative wall thickness with clinical blood pressure and with 24 hr recordings (home, work, and sleep) in 19 normal subjects and 81 patients with mild hypertension. Only a weak correlation was observed in the entire group between left ventricular mass index and clinical measurements of systolic and diastolic blood pressure (r = .24, p < .02; r = .20, p < .05, respectively), which was only slightly improved by use of systolic and diastolic blood pressure readings taken in the home (r = .31, p < .005; r = .21, p < .05, respectively). Sleep and total 24 hr blood pressure also related poorly to left ventricular mass index. In contrast, substantially higher correlations existed between left ventricular mass index and systolic and diastolic blood pressure measured by portable recorder in 60 subjects at work (r = .50, p < .001; r = .39, p < .01, respectively). Similarly, work diastolic blood pressure bore the closest relationship to relative wall thickness (r = .59, p < .001). Home blood pressure readings taken on a work day also showed a moderate relationship with indices of LVH, whereas weaker correlations were found in employed subjects whose blood pressure was recorded on a non-workday, and no relationship between blood pressure and LVH existed in subjects who were not employed. We conclude that hypertensive LVH is poorly related to clinical or home measurements of blood pressure but that a substantially closer relationship exists between LVH and blood pressure during recurring stress at work and between LVH and home blood pressure on a workday. Thus hypertensive cardiac hypertrophy appears to be more closely related to blood pressure during stressful Circulation 68, No. 3, 470-476, 1983. NUMEROUS STUDIES have demonstrated that the risk of disease and death increases as blood pressure rises.'4 However, despite the consistency of this finding and its high statistical significance in large populations, the actual correlations between blood pressure measurements and the incidence of morbid events have generally been relatively low.'4 One possible explana-

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The effects of rat atrial tissue extract on renal hemodynamics and fluid and electrolyte excretion were investigated in the isolated perfused rat kidney (IK). IK were perfused at a constant effective perfusion pressure of about 90 mmHg. After control clearance periods (C), extracts of rat atria (AE) or ventricles (VE) were added to the perfusate and three 10-min experimental periods followed. AE, but not VE, significantly increased (P less than 0.001) renal vascular resistance (RVR) to 133 +/- 8% of C, GFR to 201 +/- 34%, filtration fraction to 245 +/- 41%, urine flow (V) to 675 +/- 131%, fractional excretion (FE) of H2O to 336 +/- 29%, absolute Na excretion (UNaV) to 1,259 +/- 290%, FENa to 642 +/- 129%, UKV to 2,226 +/- 1,237%, and FEK to 542 +/- 119%. Despite the marked natriuresis, since GFR doubled, Na reabsorption rose from 78.3 +/- 36.3 in C to 132 +/- 36.3 mueq/min after AE. The effects of AE were immediate and lasted to the end of the perfusion. The lower the initial control GFR, the larger was the AE-induced increase in GFR. Perfusion with low [Ca] (0.2 mM) or verapamil (10(-5) M) severely blunted the hemodynamic, diuretic, kaliuretic, and natriuretic effects of AE. AE decreased rather than increased the RVR when IK were perfused with vasoconstrictors such as angiotensin II, norepinephrine, or vasopressin. The results demonstrate that AE acts directly on the kidney, eliciting powerful Ca-dependent hemodynamic and natriuretic responses. The natriuresis induced by AE can be accounted for, at least in part, by its renal hemodynamic effects rather than by the presence of a putative tubular natriuretic factor. The hypothesis is advanced that AE contains a substance(s) which behaves as a functional agonist/antagonist of endogenous vasoconstrictors with a preferential site of action on the efferent arterioles of the renal vasculature.

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