Quercetin had a biphasic effect on Ca 2؉ uptake and calcium-stimulated ATP hydrolysis in isolated cardiac sarcoplasmic reticulum (SR). Stimulation of Ca 2؉ATPase was observed at low quercetin concentrations (<25 M) followed by inhibition at higher concentrations. The effects were dependent upon the SR protein concentration, the MgATP concentration, and intact phospholamban regulation of cardiac Ca
SUMMARY Synthetic atrial natriuretic factor (Arg-Arg-Ser-Ser-Cys-Phe-Gly-Gly-Arg-Ile-AspArg-Ile-Gly-Ala-Gln-Ser-GIy-Leu-Gly-Cys-Asn-Ser-Phe-Arg-TVr-COOH [disulfide bond between cysteines]) was infused intravenously into conscious normotensive and deoxycorticosterone, onekidney, one-clip, and two-kidney, one-clip hypertensive rats. Mean arterial pressure, urine volume, and electrolyte excretion rates were measured during a 20-minute infusion of a single dose (ranging from 0-1520 pmol/min) into each animal; 95 to 380 pmol/minute of synthetic atrial natriuretic factor maximally reduced mean arterial pressure by -20 ± 4, -29 ± 2, and -39 ± 7 mm Hg in normotensive, one-kidney, one-clip, and two-kidney, one-clip hypertensive rats, respectively. In deoxycorticosterone rats, a dose of 760 pmol/minute was required to produce the largest depressor response (-58 ± 12 mm Hg). Sodium excretion increased to 8.8 ± 2.5 ^tEq/minute at 760 pmol/minute in normotensive rats, to 6.5 ± 1 . 1 /xEq/minute at 50 pmol/minute in deoxycorticosterone rats, and to 5.8 ± 1 . 5 /xEq/minute at 95 pmol/minute in one-kidney, one-clip animals. The natriuretic effect was consistently greater at all doses of synthetic atrial natriuretic factor in the two-kidney, one-clip hypertensive model, in which the maximum response was 15.3 ± 4.7 /xEq/minute at 190 pmol/minute. The changes in urine volume and excretion rates of potassium and chloride tended to parallel the increases in sodium excretion in each model. Interestingly, the maximally effective hypotensive dose of synthetic atrial natriuretic factor was different from the maximally effective natriuretic dose in all four groups. Even though its exact mechanisms of action remain unclear, synthetic atrial natriuretic factor appears to be an effective hypotensive and natriuretic agent in several models of conscious hypertensive rats. 1 described the biological actions of atnal extracts in anesthetized rats and reported that atnal natriuretic factor (ANF) induced a natriuretic and a hypotensive response. Shortly thereafter, a direct vasorelaxant effect of atrial preparations was demonstrated in isolated vascular smooth muscle strips.2 "* In addition, urinary guanosine cyclic 3',5'-monophosphate (cGMP) excretion and plasma cGMP concentration were elevated following injection of atrial extracts in anesthetized rats.3 A closely related group of active peptides was later isolated from rat 6 " 11 and human 12 atria, and a peptide containing a 26 amino acid sequence was synthesized l3 The structure of the synthetic ANF is as follows: Arg-Arg-Ser-Ser-CysPhe-Gly-Gly-Arg-Ile-Asp-Arg-Ile-Gly-Ala-Gln-Ser-
Synthetic atrial natriuretic factor (ANF 101-126) was infused at 1, 5, 25, and 125 pmol X kg-1 X min-1 into the renal artery of anesthetized, one-kidney dogs. During administration of 25 and 125 pmol X kg-1 X min-1 of ANF 101-126, fractional sodium excretion (FENa) rose from 1.4 +/- 0.3 to 6.6 +/- 1.1 and 5.6 +/- 1.3% when renal perfusion pressure (RPP) was at its basal level (112 +/- 5 mmHg). When base-line RPP was lowered to 101 +/- 5 mmHg by tightening a suprarenal aortic constriction, the same doses raised FENa to only 5.6 +/- 1.6 and 5.1 +/- 1.6%. A larger reduction of beginning RPP to 82 +/- 4 mmHg suppressed the natriuretic responses to 25 and 125 pmol X kg-1 X min-1 of ANF 101-126 to only 1.4 +/- 0.8 and 0.8 +/- 0.3%, respectively. During the peak natriuretic dose of 25 pmol X kg-1 X min-1, renal vascular resistance (RVR) fell from 0.88 +/- 0.10 to 0.68 +/- 0.07, from 0.78 +/- 0.10 to 0.68 +/- 0.12, and from 0.60 +/- 0.06 to 0.61 +/- 0.06 mmHg X ml-1 X min-1 at RPP = RPP = 112, 101, and 82 mmHg, respectively. ANF 101-126 did not affect glomerular filtration rate (GFR) at any level of RPP tested. In conclusion, the natriuretic responses to ANF 101-126 occurred without changes in GFR and were modulated by the prevailing levels of renal perfusion pressure and renal vascular resistance.
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