Weevaluated whether reduction in sympathetic reactivity plays a major role in the spontaneous falls in blood pressure (BP) experienced during hospitalization by patients with essential hypertension. In the present case BP fell on the 2nd day of hospitalization. The responses of plasma catecholamines (CA) and BP to both handgrip and tilting were not altered during either the first 24 hours or the entire 7 days of hospitalization. The effect of phentolamine on BPwas similar on the 1st, 2nd and 7th days. However, the resting levels of plasma norepinephrine before handgrip, tilting and phentolamine were significantly diminished on the 7th day, but not on the 2nd day. In conclusion, the diminution of sympathetic activity may be partly responsible for the hospitalization-induced fall in BPin the late stages.
To clarify the cardiovascular effects of central vasopressin (AVP), a chronic intracerebroventricular (ICV) infusion of AVP was performed in conscious Wistar normotensive rats. Animals were divided into 3 groups: 1) AVP 1 ng/hr (Low), 2) AVP 100 ng/hr (High), and 3) saline (control) ICV infusion. After a 6 day control period, AVP or saline was continuously infused into the lateral cerebroventricle at a rate of 1 microliter/hr using osmotic minipump for 7 days. As a result, a dose-related elevation of AVP concentration in CSF was achieved. Systolic blood pressure in both Low and High AVP infusion was slightly (7-12 mmHg) but significantly higher than that in control. ICV infusion of AVP did not alter urine volume, electrolytes excretion or osmolality, and AVP vascular antagonist injected intravenously failed to affect mean arterial pressure. Furthermore, plasma catecholamines and renin activity did not differ significantly among the groups. Thus, chronic ICV infusion of AVP induced the elevation of blood pressure, which is due to centrally mediated effect of AVP.
The condition that a part of the digestive tract interposes between the liver and diaphragm has been called Chilaiditi's syndrome. Although it has been reported that this condition had a higher rate of incidence in patients of mental hospitals than in other individuals, there are hardly any enlightening papers of this condition in the domain of psychiatry. Three schizophrenic patients who had this condition are described in this paper. Many factors such as meteorism, the medication of antipsychotic drugs and negative symptoms of schizophrenic patients are considered as risk factors that bring about this condition in them. Psychiatrists should pay more attention to this condition in the chest roentgenograms of patients because this state can possibly develop into more serious conditions such as ileus.
1. To determine the long-term haemodynamic and humoral effects of arginine vasopressin (AVP), a chronic intravenous infusion of AVP was performed in conscious Wistar normotensive rats. 2. AVP (1, 10, 50 or 100 ng/h) or saline as a vehicle control was infused continuously into the right jugular vein at a rate of 1 microL/h using an osmotic minipump for 7 days. 3. As a result, significant elevations of systolic blood pressure were observed in association with increases in plasma AVP concentration. Significant decreases in heart rate were observed during infusion of 100 ng/h of AVP. Mean arterial pressures measured directly on the sixth day of infusion were significantly higher in the rats given 50 ng/h (125 +/- 3 mmHg) or 100 ng/h (125 +/- 2 mmHg) compared with control rats (117 +/- 2 mmHg). Intravenous injection of the V1 antagonist, d(CH2)5Tyr(Me)AVP, significantly reduced the elevated mean arterial pressure induced by 50 or 100 ng/h of AVP (-7 +/- 4 and -11 +/- 2 mmHg, respectively). Plasma renin and norepinephrine concentrations were not affected by AVP infusion, while plasma epinephrine concentration was lower in the rats given 100 ng/h of AVP. Intravenous infusion of AVP did not alter bodyweight, serum electrolytes or osmolality. 4. These results suggest that AVP has a long-term pressor effect which is attributable to its vasoconstrictor action in conscious rats.
Nifedipine was administered orally to 2 patients with primary hyperparathyroidism before and after parathyroidectomy. The operation lowered serum calcium concentration and parathyroid hormone but did not alter plasma renin activity, plasma aldosterone concentration, and serum magnesium. The hypotensive effects of nifedipine were markedly enhanced with the decrease in serum calcium concentration following parathyroidectomy. Thus, the level of serum calcium concentration may modulate the hypotensive effect of nifedipine in humans.
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