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authors request that the following corrections be noted.In this paper, a calculation was presented of tdc, a mean capture time for those low density lipoprotein (LDL) receptors trapped by a coated pit during the lifetime of the coated pit. However, the appropriate mean capture time for this problem must also take into account LDL receptors that are not captured during any single lifetime of a coated pit. When this is done, the mean capture time becomeswhere f is the fraction of LDL receptors trapped during the lifetime of a coated pit. The fractionf is given by the expression f r(bv 2 1 r(r)dr= (b2 2al where a = \/K72 and v(r), E1, and A10 are given in the Appendix of the paper. Corrections

Abstract-There is growing evidence that essential hypertension is commonly neurogenic and is initiated and sustained by sympathetic nervous system overactivity. Potential mechanisms include increased central sympathetic outflow, altered norepinephrine (NE) neuronal reuptake, diminished arterial baroreflex dampening of sympathetic nerve traffic, and sympathetic neuromodulation by angiotensin II. To address this issue, we used microneurography and radiotracer dilution methodology to measure regional sympathetic activity in 22 hypertensive patients and 11 normotensive control subjects. The NE transport inhibitor desipramine was infused to directly assess the potential role of impaired neuronal NE reuptake. To evaluate possible angiotensin sympathetic neuromodulation, the relation of arterial and coronary sinus plasma concentrations of angiotensin II to sympathetic activity was investigated. Hypertensive patients displayed increased muscle sympathetic nerve activity and elevated total systemic, cardiac, and renal NE spillover. Cardiac neuronal NE reuptake was decreased in hypertensive subjects. In response to desipramine, both the reduction of fractional transcardiac 3[H]NE extraction and the increase in cardiac NE spillover were less pronounced in hypertensive patients. DNA sequencing analysis of the NE transporter gene revealed no mutations that could account for reduced transporter activity. Arterial baroreflex control of sympathetic nerve traffic was not diminished in hypertensive subjects. Angiotensin II plasma concentrations were similar in both groups and were not related to indexes of sympathetic activation. Increased rates of sympathetic nerve firing and reduced neuronal NE reuptake both contribute to sympathetic activation in hypertension, whereas a role for dampened arterial baroreflex restraint on sympathetic nerve traffic and a peripheral neuromodulating influence of angiotensin II appear to be excluded. Key Words: hypertension, essential Ⅲ catecholamines Ⅲ sympathetic nervous system Ⅲ norepinephrine Ⅲ angiotensin II A lthough there is growing evidence that essential hypertension is commonly neurogenic 1,2 and is initiated and sustained by overactivity of the sympathetic nervous system, the precise causal mechanisms leading to sympathetic augmentation in hypertensive subjects are still poorly understood. Among others, possible mechanisms include increased sympathetic nerve firing rates, 1,2 altered neuronal norepinephrine (NE) reuptake, 3,4 diminished arterial baroreflex buffering of sympathetic nerve traffic, 5 and facilitation of NE release by neurohumoral factors such as angiotensin II. 6 These possibilities, however, have not yet been conclusively tested for in humans.To further address some of these issues, we combined microneurography, to measure sympathetic nerve firing rates, with relevant radiotracer methodology to comprehensively study systemic and regional kinetics of NE and its intraneuronal and extraneuronal metabolites. To directly assess whether decreased neuronal NE reuptake contributes ...