Toshio Nishikimi

Effect of exercise on circulating atrial natriuretic polypeptide in valvular heart disease

Abstract The atrial peptides that have potent natriuretic, diuretic and vasodilatory effects have been purified from human tissues and their structures have been determined.1 Also, it has been shown that acute volume expansion causes an immediate increase in plasma concentration of immunoreactive atrial natriuretic polypeptide (ANP) in rats.2 These data imply that ANP is secreted from cardiac atria, presumably by the stimulation of atrial stretch receptor. We measured plasma ANP concentrations during 3 grades of exercise (25, 50 and 75 W) on a bicycle ergometer in 6 patients with valvular heart disease.

An angiotensin II receptor antagonist attenuates left ventricular dilatation after myocardial infarction in the hypertensive rat

OBJECTIVE The aims were (1) to investigate the effect of hypertention on left ventricular dilatation and haemodynamic alterations following acute myocardial infarction in spontaneously hypertensive rats (SHR) and normotensive rats (WKY); (2) to compare haemodynamic indices between the two groups; (3) to assess whether the angiotensin II type 1 receptor antagonist (AIIA), TCV-116, prevented left ventricular dilatation after myocardial infarction; and (4) to compare the effect of AIIA with that of the angiotensin converting enzyme (ACE) inhibitor, delapril. METHODS Myocardial infarction was produced in SHR and WKY by coronary artery ligation. Haemodynamic measurements were obtained three weeks later in rats that had been treated from the next day after the operation for three weeks with TCV-116 (1 mg.kg-1.d-1) or delapril (1 g.litre-1 in drinking water), and in untreated controls. RESULTS After myocardial infarction, left ventricular weight, and left ventricular weight were greater in SHR than in normotensive rats. Right ventricular weight, left ventricular end diastolic pressure, and LVEDVI correlated positively with infarct size in both SHR and WKY and these slopes were steeper in SHR than in WKY (P < 0.05). TCV-116 and delapril each significantly attenuated the increases in left ventricular end diastolic pressure, left ventricular weight, right ventricular weight, and LVEDVI following myocardial infarction in both in WKY and SHR, and shifted pressure-volume curve significantly to the left. CONCLUSIONS Hypertension accelerates left ventricular dilatation and haemodynamic alterations following myocardial infarction in rats. These effects are attenuated by an angiotensin II type 1 receptor antagonist as well as by an ACE inhibitor.

Influence of exercise on plasma atrial natriuretic favor levels in patients with myocardial infarction

The influence of dynamic exercise on plasma atrial natriuretic factor (ANF) levels was studied in a group of 10 patients with myocardial infarction (MI) and five patients with atypical chest pain (control group). Exercise protocol consisted of three fixed workloads (25, 50, and 75 watts) every 4 minutes with the use of a supine bicycle ergometer. Plasma ANF levels and hemodynamic indices were measured before, during, and 10 minutes after exercise. In the MI group, plasma ANF levels significantly increased at the 75-watt workload and significantly decreased at 10 minutes after exercise, whereas in the control group, the increase in plasma ANP levels after a 75-watt workload, compared with those at rest, was not significant. Significant correlations of pulmonary artery wedge pressure, right atrial pressure, mean arterial pressure, and heart rate to plasma ANF levels were observed at four points obtained before and during each stage of exercise in the MI group. Furthermore, a significant correlation between maximal creatine kinase levels and plasma ANF levels at a 75-watt workload and a significant inverse correlation between left ventricular ejection fraction and plasma ANF levels at a 75-watt workload were observed. These results suggest that the increase in the circulating ANF level during exercise in MI is associated with elevated atrial pressure resulting from left ventricular dysfunction and that measurement of ANF during exercise may be an indication of the severity of MI and associated left ventricular dysfunction.

Influence of Nisoldipine on Hemodynamics and Atrial Natriuretic Polypeptides at Exercise Loading in Hypertensive Patients

The effect of a calcium antagonist, nisoldipine, on cardiac hemodynamics and the response of atrial natriuretic polypeptides (ANP) were investigated at exercise loading in hypertensive patients. A dose of 5 mg nisoldipine was administered to seven patients with untreated essential hypertension. Multistage exercise loading (25 W, 50 W, and 75 W) was performed before and after administration on a supine bicycle ergometer for 4 min at each exercise stage. Heart rate, blood pressure, pulmonary artery pressure (PAP), and pulmonary artery wedge pressure (PAWP) were measured at rest and at each exercise stage under catheterization using a Swan-Ganzcatheter. At the same time, blood samples were collected from the pulmonary artery for measurement of ANP. Radioimmunoassay, as we reported previously, was used in the measurement of ANP (1986), (Biochem Biophys Res Commun 134: 178–183).

Pseudo-Coarctation of the Abdominal Aorta Associated with Renovascular Hypertension

A case of pseudo-coarctation of the abdominal aorta associated with renov ascular hypertension has been reported. The abdominal aorta of the patient was kinked at the level of L1-L2 without a pressure gradient, which was consistent with pseudo-coarctation of aorta. Both renal arteries arose from the aorta at the level of lower T12 and had severe multiple stenoses. We have discussed the possible etiology of the developmental abnormalities of the arterial system in this patient.