Hemodynamic and renal responses to physiological levels of atrial natriuretic factor in conscious dogs.

The effects of increases in plasma atrial natriuretic factor (ANF) similar to those encountered after rapid volume expansion were examined in conscious dogs. Hemodynamics and renal function were continuously monitored during 30 minutes of human ANF infusion (10 ng/kg.min) and throughout a 30-minute recovery period. Ten minutes into the infusion period, plasma levels of ANF were elevated (p less than 0.01) by 34 +/- 9 from 36 +/- 5 pg/ml and sodium excretion increased (p less than 0.05) by 34 +/- 7 from 67 +/- 9 mueq/min. At that time, urine flow did not differ from baseline (0.25 +/- 0.03 ml/min). Renal blood flow velocity fell (p less than 0.01) by 5.0 +/- 0.5 from 42.3 +/- 3.7 cm/sec. Thirty minutes into the infusion period, plasma ANF levels were increased (p less than 0.01) by 61 +/- 9 pg/ml, similar to levels found after rapid volume expansion in conscious dogs. Urine flow and sodium excretion were elevated (p less than 0.01) by 0.35 +/- 0.06 ml/min and by 65 +/- 12 mueq/min, respectively. Renal blood flow velocity was reduced (p less than 0.05) by 4.4 +/- 1.5 cm/sec. Neither right atrial pressure, left ventricular end-diastolic pressure, mean arterial pressure, the first derivative of left ventricular pressure over time (dP/dt), nor heart rate were influenced by the elevated ANF plasma levels. Circulating levels of vasopressin and aldosterone were unaltered by these increases in plasma ANF. Thirty minutes into the recovery period, all variables were similar to the preinfusion baseline. Thus, in conscious dogs, physiologically relevant increases in plasma levels of ANF reached diuretic and natriuretic thresholds.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary dilation with carotid chemoreceptor stimulation in cardiac-denervated dogs.

The coronary vasodilation that is secondary to carotid chemoreceptor stimulation (CCS) was compared in normal (N) and in cardiac-denervated (CD) conscious dogs. Under base-line conditions, CD only differed from N dogs by greater (P less than 0.01) increases in mean arterial pressure (MAP) with CCS. Coronary blood flow (CBF) increased similarly in N (146 +/- 18%) and CD (126 +/- 15%) dogs, and coronary resistance (CR) fell to a similar extent in N (53 +/- 3%) and CD (43 +/- 5%) dogs. After muscarinic and beta-adrenergic blockade, CCS resulted in similar increases in MAP in N and CD dogs; increases in CBF averaged 122 +/- 15 and 115 +/- 12% in N and CD dogs, respectively. Decreases in CR with CCS averaged 46 +/- 3 and 40 +/- 5% in N and CD dogs, respectively. alpha 1-Adrenergic blockade prevented the increases in MAP with CCS and resulted in smaller (P less than 0.01) increases in CBF, similar in N (77 +/- 13%) and in CD (69 +/- 10%) dogs. CR fell to the same extent in N (40 +/- 4%) and CD (37 +/- 5%) dogs. Additional blockade of alpha 2-adrenergic receptors further limited the increases in CBF with CCS in N (20 +/- 5%) and CD (28 +/- 7%) dogs; decreases in CR were attenuated similarly in N (13 +/- 5%) and CD (21 +/- 5%) dogs. Thus, in conscious dogs, cardiac nerves contribute little to the coronary dilation after carotid chemoreceptor stimulation.

Hemodynamic and renal responses to volume expansion in dogs with cardiac denervation.

Hemodynamic responses, renal function, and plasma levels of immunoreactive atrial natriuretic factor (irANF) were examined following volume expansion (VE) in normal (N) conscious dogs and in conscious dogs with cardiac denervation (CD). Base-line urine flow was consistently greater (P less than 0.05) in dogs with CD (0.54 +/- 0.06 ml/min) than in N (0.29 +/- 0.03 ml/min) dogs but sodium excretion did not differ between N (2.80 +/- 0.58 mu eq.min-1.kg body wt-1) and CD (3.53 +/- 0.75 mu eq.min-1.kg-1) groups. With VE (18 ml/kg of 3% dextran in saline), mean arterial pressure (MAP) increased (P less than 0.01) by 16 +/- 3 from 103 +/- 4 mmHg in N dogs but did not change from pre-VE base line (103 +/- 2 mmHg) in dogs with CD. At 10 min after VE, urine flow increased more (P less than 0.01) in N dogs (1.39 +/- 0.24 ml/min) than in dogs with CD (0.26 +/- 0.09 ml/min). At that time, increases in sodium excretion were also greater (P less than 0.01) in N (9.13 +/- 1.96 mu eq.min-1.kg-1) dogs than in dogs with CD (1.06 +/- 0.68 mu eq.min-1.kg-1). With VE, increases in irANF plasma levels were not different in N dogs (40 +/- 12 from 34 +/- 5 pg/ml) and in dogs with CD (27 +/- 3 from 45 +/- 7 pg/ml). In dogs with CD, when MAP was increased by aortic constriction to mimic responses observed in N dogs, renal responses were similar to those of N dogs.(ABSTRACT TRUNCATED AT 250 WORDS)