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Biomedical subjects

K Kamoi

Publications and source records attributed to K Kamoi.

At least 127 records · Page 7Linked to original sources
PubMed1982

Central role of angiotensin in the hyperosmolality- and hypovolaemia-induced vasopressin release in conscious rats.

To evaluate a central role of angiotensin in vasopressin (ADH) release in response to hyperosmolality or hypovolaemia, we examined in conscious rats the effects of intraperitoneal (ip) injections of 2 ml/100 g body weight of hypertonic saline or polyethylene glycol (PEG; 250 mg/ml of 145 mM NaCl) on plasma ADH and angiotensin II (AII) levels and of intracerebroventricular (icv) administrations of Sar1-Ala8-AII (a competitive receptor blocker for AII) on the plasma ADH responses to the ip injections. Thirty min after ip injections of 900 mM NaCl, plasma ADH, osmolality and sodium increased with unchanged plasma AII and with reduced haematocrit. Two h after ip administrations of PEG, plasma ADH, AII and haematocrit were augmented with unaltered plasma osmolality and sodium. The responses of plasma ADH to ip injections of 900 mM NaCl and PEG were significantly inhibited (P less than 0.05) by 1 microgram of Sar1-Ala8-AII injected icv 5 min before blood samplings which had no appreciable effect on plasma osmolality, electrolytes and haematocrit. Based on these results, we concluded that angiotensin may participate in both the hyperosmolality- and hypovolaemia-induced ADH secretion by acting on the central nervous system.

Angiotensin II↗
PubMed1981

Effect of nephrectomy on angiotensin II concentrations in plasma and hypothalamus of the dehydrated rat.

Bilateral nephrectomy in the rats deprived of water for 46 h markedly reduced plasma angiotensin II concentrations (P less than 0.001), but it was without effect on extremely low levels of the hormone in the hypothalamic tissue. These results may suggest that the activity of a possible intrinsic brain renin-angiotensin system is not influenced by that of the kidney-plasma renin-angiotensin system.

Angiotensin II↗
PubMed1981

[Effects of baroregulation on osmoregulation of arginine vasopressin in rats (author's transl)].

A relationship between blood pressure and the functional character of osmoreceptor controlling vasopressin secretin under usual physiological situations in the rat was studied by employing Na-nitroprusside as depressor agent or norepinephrine as pressor agent and the sensitive and specific radioimmunoassay of arginine vasopressin (AVP). Na-nitroprusside or control saline was given s.c. 15 min after an i.p. injection of 2% (v/w) hyper, hypo or isotonic saline. Norepinephrine or control saline was given s.c. with a concurrent i.p. injection of 2% (v/w) hyper, hypo or isotonic saline. 30 min after this osmotic load, plasma AVP (pAVP) and osmolality (pOSM) were measured on trunk blood as previously described (J. Clin. Invest. 52: 3212, 1973). In rats given Na-nitroprusside, 2 mg/kg body weight, osmotic loading produced a rise in pAVP which correlated relationship (pAVP=1.9 [pOSM-276.6]; N=16; r=0.81) raised significantly (p less than 0.001) to the left of that in the control vehicle (pAVP=1.4[pOSM,-293.8]; N=8; r=0.86). In rats given norepinephrine, 0.1 mg/kg body weight, the regression line generated by osmotic loading (pAVP=1.2[pOSM-229]; N=7; r=0.88) fell significantly (p less than 0.001) to the right of that in the control vehicle (pAVP=1.4[pOSM-202]; N=6; r=0.99). In 4 rats, the same dose of Na-nitroprusside and norepinephrine resulted in a significant (p less than 0.001) decrease (40%) and increase (20%) from the basal level for the same time of osmotic loading in mean arterial blood pressure as measured directly via chronically implanted aorta catheters, respectively. These results indicate that hypotension increases pAVP by lowering the threshold or set and increasing the sensitivity of the osmoregulatory system and hypertension decreases pAVP by raising the threshold or set and reducing the sensitivity of the mechanism without abolishing the system.

Animals↗
PubMed1981

Comparison of the responses in the nomifensine test with hyperprolactinemia due to prolactin-secreting pituitary tumors and nonprolactin-secreting hypothalamic tumors.

It has recently been proposed that nomifensine (Nom) administration discriminates those patients with PRL-secreting pituitary tumors from those who have hyperprolactinemia due to other causes. In the present study, this test was performed on 12 presumed functional hyperprolactinemic subjects, 9 patients with surgically proved PRL-secreting pituitary adenoma (6 microadenoma and 3 macroadenoma), and 7 patients with surgically proved non-PRL-secreting hypothalamic tumors (3 craniopharyngioma, 3 suprasellar germinoma, and 1 suprasellar ependymoma). The Nom test suppressed the plasma PRL level to below 60% of the basal level in all 12 women with presumed functional hyperprolactinemia, but did not alter plasma PRL levels in the patients with PRL-secreting pituitary adenoma or hypothalamic tumor. This evidence confirms that the test is, at least in part, able to discriminate those individuals with PRL-secreting pituitary adenoma from those without, regardless of the size of the tumor. However, the test is not capable of distinguishing between hyperprolactinemia due to PRL-secreting pituitary tumors and that due to non-PRL-secreting hypothalamic tumors. A lack of response to Nom is not necessarily due to the presence of a PRL-secreting tumor, and may be related to dysfunction to the hypothalamic-pituitary system.

Adenoma↗
PubMed1981

[Eugenol cement].

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Dental Cavity Lining↗