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Featured researches published by Jeanette Shinsako.


Brain Research | 1987

The suprachiasmatic nuclei stimulate evening ACTH secretion in the rat

Caren S. Cascio; Jeanette Shinsako; Mary F. Dallman

The effect of bilateral lesions of the suprachiasmatic nuclei (SCN) on the circadian rhythm in ACTH was studied in rats that were adrenalectomized and implanted with a subcutaneous corticosterone (B) pellet. Rats wee chronically cannulated to allow for repeated blood sampling. In rats with B pellets, bilateral lesions of the SCN eliminated the circadian rise in plasma ACTH seen in sham-lesioned animals. This is consistent with the idea that the SCN stimulate ACTH secretion in the evening.


Neuroendocrinology | 1989

Role of Alpha-Adrenergic Mechanism in Effects of Morphine on the Hypothalamo-Pituitary-Adrenocortical and Cardiovascular Systems in the Rat

Shuso Suemaru; Mary F. Dallman; Daniel N. Darlington; Caren S. Cascio; Jeanette Shinsako

The role of alpha-adrenergic mechanism in the acute effects of morphine in the hypothalamo-pituitary-adrenocortical (HPA) and cardiovascular (CV) systems, and the interrelationship between the HPA and CV responses to alpha-adrenoceptor antagonists and/or morphine were studied by peripheral administration of prazosin, a selective alpha 1-adrenoceptor antagonist, and yohimbine, a selective alpha 2-adrenoceptor antagonist, in conscious, unstressed or ether-stressed rats. The test substances were administered intravenously or intraperitoneally in chronically cannulated or noncannulated rats. In the i.v. experiment, morphine (1 mg/100 g BW) rapidly induced a pronounced bradycardia and a short-lasting fall in blood pressure (BP), followed by a rise in BP, and increased plasma corticosterone concentration. Prazosin (0.5 mg/kg BW) induced a rapid fall in BP and tachycardia, and increased plasma corticosterone concentration. Pretreatment with prazosin did not block the effect of morphine on the CV system, but abolished the morphine-induced increment in plasma corticosterone concentration. Yohimbine (0.5 mg/kg BW) induced a rapid and a subsequent slowly developing rise in BP and tachycardia, and increased plasma corticosterone concentration. Pretreatment with yohimbine did not block the effect of morphine on the CV system nor alter the stimulatory effect of morphine on the secretion of corticosterone. In the intraperitoneal experiment, morphine (2 mg/100 g BW) stimulated the secretion of adrenocorticotropic hormone (ACTH) and corticosterone and prazosin (1 mg/kg BW) stimulated the secretion of corticosterone, but pretreatment with prazosin reduced the morphine-induced increment in plasma corticosterone concentration in unstressed rats. In stressed rats, morphine reduced the stress-induced increment in plasma ACTH and corticosterone concentrations and prazosin also reduced the stress-induced increment in plasma corticosterone concentration. Pretreatment with prazosin did not alter the inhibitory effect of morphine...


Brain Research | 1988

Paraventricular lesions: hormonal and cardiovascular responses to hemorrhage

Daniel N. Darlington; Jeanette Shinsako; Mary F. Dallman

The responses of adrenocorticotropin (ACTH), renin, epinephrine and norepinephrine and arterial pressure and heart rate (HR) to hypotensive hemorrhage were examined before and 1 h after lesion of the paraventricular nuclei (PVN) in pentobarbital-anesthetized rats and 1 day before and 4 days after lesion of the PVN in conscious rats. The ACTH response to hemorrhage was abolished 1 h (n = 8) and 4 days (n = 14) after PVN lesion whereas the ACTH response in the sham groups (in both anesthetized and conscious studies, n = 8 and 16 respectively) remained intact. PVN lesion had no effect on basal ACTH levels 4 days after lesion. The responses of renin, epinephrine, norepinephrine and mean arterial blood pressure (MABP) and HR to hemorrhage were not affected 1 h or 4 days after PVN lesion. Resting levels of the above variables did not change 4 days after lesion. The PVN lesion had a small (but significant) effect on the baroreceptor reflex in the conscious study (reflex changes in HR caused by phenylephrine- or nitroglycerin-induced change in MABP) and had no effect on the baroreceptor reflex in the anesthetized study. The group with PVN lesions gained more weight 6 days after lesion than the group with sham lesions. We conclude that the PVN are part of a neural pathway involved in ACTH regulation during perturbations of the cardiovascular system and on weight gain and that PVN lesions have little or no effect on resting or stimulated (hemorrhage) levels of renin, epinephrine, norepinephrine, HR and MABP or on the baroreceptor reflex.


Experimental Biology and Medicine | 1983

Surgery Potentiates Adrenocortical Responses to Hypoxia in Dogs

Hershel Raff; Jeanette Shinsako; Mary F. Dallman

Abstract We studied the effect of prior surgery on the ACTH and corticosteroid responses to acute hypoxia. Five conditioned, pentobarbital-anesthetized, gallamine-paralyzed mongrel dogs were exposed to 24 min of isocapnic hypoxia (11% O2/89% N2) 2 hr (Expt I) and approximately 1 week (Expt II) after implantation of femoral arterial and venous catheters. ACTH and corticosteroid responses were assessed by RIA of arterial plasma samples. Arterial PO2 fell similarly in both experiments from 82 to 26 Torr. This caused significant increases in ACTH of similar magnitude in both experiments. Corticosteroid levels increased more in Expt I than Expt II indicating an apparent potentiation by surgery of the adrenocortical response to hypoxia. Two additional dogs were studied in reverse order under lighter anesthesia such that ACTH and corticosteroid levels after surgery were higher than in the first set of experiments. Under these conditions, hypoxia still produced a large increase in ACTH and corticosteroids after acute surgery. Correlation of log ACTH with corticosteroid levels (adrenal dose response) revealed a significant increase in slope in dogs with acute surgery suggesting that surgery interacted with hypoxia either to change the metabolic clearance rate of corticosteroid or to increase adrenal sensitivity to ACTH.


Analytical Biochemistry | 1967

Gas chromatographic method for the determination of testosterone in urine

Laurence C. Wegienka; Bruce F. Bower; Jeanette Shinsako; Tawfik M. Elattar; Satoshi Hane; Neva Mimica; Elena Demertze; Jane E. Stutheit; Peter H. Forsham

Abstract A method is described for measuring testosterone in the urine using glucuronidase hydrolysis, continuous extraction with methylene dichloride, and chromatography on silica gel column as well as thin-layer and gas chromatography. This method proved to be practical for processing large numbers of samples and gave consistently reproducible results in the more than 600 specimens tested in the course of clinical evaluation of patients.


Molecular Endocrinology | 1998

Estrogen Receptor Activation Function 1 Works by Binding p160 Coactivator Proteins

Paul Webb; Phuong Nguyen; Jeanette Shinsako; Carol M. Anderson; Weijun Feng; Mimi P. Nguyen; Dagang Chen; Shih-Ming Huang; Sujatha Subramanian; Eileen McKinerney; Benita S. Katzenellenbogen; Michael R. Stallcup; Peter J. Kushner


Endocrinology | 1981

Adrenal Sensitivity to Adrenocorticotropin Varies Diurnally

Masanori Kaneko; Kuniko Kaneko; Jeanette Shinsako; Mary F. Dallman


American Journal of Physiology | 1978

Angiotensin II infusion increases vasopressin, ACTH, and 11-hydroxycorticosteroid secretion

David J. Ramsay; Lanny C. Keil; Michael Sharpe; Jeanette Shinsako


Endocrinology | 1982

Pituitary-Adrenal Function in Rats Chronically Exposed to Cold

Joan Vernikos; Mary F. Dallman; Candy Bonner; Alisa Katzen; Jeanette Shinsako


Endocrinology | 1988

Circadian Variations in Plasma Corticosterone Permit Normal Termination of Adrenocorticotropin Responses to Stress

Lauren Jacobson; Susan F. Akana; Caren S. Cascio; Jeanette Shinsako; Mary F. Dallman

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Susan F. Akana

University of California

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Charles E. Wade

University of Texas Health Science Center at Houston

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