PURPOSE:To develop a minimum set of analyses and a format for presentation of outcomes of astigmatism correction by laser systems that reshape the cornea.

Stereoacuity was not different at distance and near under normal viewing conditions. The conflict between subject knowledge of target proximity and the optically-induced relaxation of accommodation and convergence, or an inaccurate accommodative-convergence response, might have caused poor near-compensated stereoacuity.

The mechanisms responsible for abnormal fluid retention in congestive heart failure (CHF) are unclear. Studies were conducted to elucidate how endothelin (ET) may contribute to salt and water retention. Cardiomyopathic (CM) hamsters with moderate heart failure were employed for in vivo and in vitro trials. Clearance methods were used to compare the level of renal function in CM hamsters and control animals. Radioligand binding studies were also performed to determine ET receptor distribution in the inner medullary collecting ducts. CM hamsters exhibited an attenuated response to ANF infusion (FE_Na: 2.7 ± 0.5 vs. 5.9 ± 0.8%, p < 0.01; FE_H2O: 1.7 ± 0.3 vs. 3.2 ± 0.4%, p < 0.01; U_cGMP: 11.2 ± 2.3 vs. 16.6 ± 2.0 pmol/min, p < 0.05) and a decrease in total ET receptor density (532 ± 77 vs. 959 ± 154 fmol/mg protein, p < 0.005). Particularly ET_B receptors were significantly reduced (214 ± 26 vs. 483 ± 88 fmol/mg protein, p < 0.003). Enalapril therapy simultaneously restored the natriuretic and diuretic effects of ANF and ET receptor density in the diseased animals. These studies suggest that the renin-angiotensin-aldosterone system and ET hormonal system act together, via ET_B receptor downregulation, to promote the abnormal fluid retention observed in CHF.

Previous studies have shown that endothelin (ET) antagonizes the actions of arginine vasopressin (AVP) in the renal collecting ducts. On the other hand, the effects of AVP on ET function within the collecting ducts of the kidney have not been investigated extensively. Using isolated inner medullary collecting ducts (IMCD), we examined the possibility that a decrease in ET(B) receptor mRNA accompanied AVP-induced downregulation of ET(B) receptors. Binding studies revealed that overnight incubation of rat IMCD cells with AVP significantly reduced the maximal binding capacity (B(max)) of ET. Activation of adenylate cyclase by forskolin decreased the total ET(B) receptor density by approximately 42% but did not affect the density of ET(A) receptors. The Rp diastereoisomer of adenosine 3', 5'-cyclic monophosphothionate, Rp-cAMPS (a specific inhibitor of protein kinase A), blocked the AVP-induced reduction in ET receptor density. Using competitive PCR method, we also observed downregulation of ET(B) receptor mRNA in IMCD treated with AVP. Additional studies were done with IMCD to determine whether AVP inhibited the ET-induced accumulation of cGMP. We saw a reduction in ET-induced cGMP accumulation when IMCD was incubated overnight with AVP. This inhibition of ET-induced accumulation of cGMP was blocked by Rp-cAMPS. These results suggest that AVP regulates ET(B) receptor expression in IMCD.