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Biomedical subjects

A Grossman

Publications and source records attributed to A Grossman.

331 records · Page 19Linked to original sources
PubMedDate not supplied

Hemodynamic actions of a synthetic atrial natriuretic factor.

The recently discovered atrial natriuretic factor (ANF), as well as synthetic ANF, has been demonstrated to produce diuresis and vasodilation. However, the vascular actions appear to be selective. In view of this apparent relative specificity, the hemodynamic actions of synthetic ANF (atriopeptin II, 23 amino acid rat sequence) were examined in intact animals and in vascular beds as well as in isolated cardiac preparations. Administration of 1-100 micrograms/kg of ANF i.v. into conscious spontaneously hypertensive rats (SHRs) resulted in a dose-related fall in blood pressure. Heart rate decreased at the lowest dose. Cardiac output was depressed. Infusion of 1 microgram/kg/min also reduced blood pressure and decreased cardiac output slightly (approximately 15%). Intraarterial (i.a.) administration or i.v. injection of ANF into the blood supply of a kidney of anesthetized SHRs augmented renal blood flow and reduced renal vascular resistance. In contrast, i.a. administration into the hindquarters failed to increase blood flow or decrease resistance of this bed significantly. The specific dopamine1 (DA1)-receptor agonist SKF 82526 was examined for comparative purposes and was found to augment both renal and hindquarter blood flow following i.a. administration. The renal vasodilator actions of SKF 82526 but not ANF were antagonized by the specific DA1-receptor blocker SCH 23390 (hindquarter effects were not evaluated). ANF did not affect the force of contraction or rate of beating of isolated guinea pig atria or isolated hearts and therefore does not appear to possess direct inotropic or chronotropic properties. In conclusion, ANF lowered blood pressure in conscious SHRs; the lowering of pressure was accompanied by a slight fall in cardiac output, but there was no reflex tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Corticotropin-releasing hormone: interactions with the immune system.

Communication between the neuroendocrine and immune systems is crucial to host defence in both health and disease. Stress adversely interferes with the function of the immune system but the mechanism of such stress-induced immunosuppression is not well understood. Corticotropin-releasing hormone (CRH) is a 41-amino residue peptide which primarily stimulates ACTH secretion. In addition, CRH integrates a series of responses during the stress response. Over the last few years increasing evidence has suggested that CRH, the major stress-integrating peptide, may also directly modulate immune system function. Thus, recent data have demonstrated that CRH acts centrally as an immunosuppressant agent independent of circulating glucocorticoids. This central immunosuppressive effect of CRH is mediated at least partly via the central stimulation of sympathetic outflow. At a peripheral level, the presence of CRH and CRH receptors within cells of the immune system, and its complex effects directly on immune function, suggest that CRH is intimately associated with communication between the neuroendocrine and immune systems.

Adaptation, Physiological↗
PubMedDate not supplied

Specific binding of 3H-estradiol to the cytosol of rat pancreas and uterus: bound sites in pancreatic extracts do not translocate 3H-estradiol to nuclei suggesting a basic difference in mode of action.

In parallel sets of experiments, cytosol fractions from rat pancreas and uterus were incubated with 2 nM 3H-estradiol in the presence or absence of nuclei from pancreas and liver. After incubation for 1 hr at room temperature, the nuclei were removed by centrifugation and specific binding determined in the cytosol fractions as well as in the separated nuclei. The protein that binds 3H-estradiol in uterine extracts translocated the hormone to nuclei of pancreas and liver while the one in pancreas was devoid of this activity. It is presumed, therefore, that modification of transcription is not a primary action of the steroid-bound complex in pancreas.

Animals↗
PubMedDate not supplied

Virtuous capital: what foundations can learn from venture capitalists.

U.S. foundations and nonprofits work diligently on behalf of society's most needy and yet report that progress is slow and social problems persist. How can they learn to be more effective with their limited resources? Foundations should consider expanding their mission from investing only in program innovation to investing in the organizational needs of nonprofit organizations as well. Their overemphasis on program design has meant deteriorating organizational capacity at many nonprofits. If foundations are to help nonprofits be assured of making payroll, paying the rent, or buying a much-needed computer, they must develop hands-on partnering skills. Venture capital firms offer a helpful benchmark. In addition to putting up capital, they closely monitor the companies in which they have invested, provide management support and stay involved long enough to see the company become strong. If foundation officers familiarize themselves with such practices, they can begin to build organizational capacity in the nonprofit sector. Foundations can hire organizational experts to assist grantees; they can lengthen grant terms to allow nonprofits to build up organization strengths; and they can create new classes of grants that allow for organizational effectiveness. Nonprofits in turn should articulate their organizational needs when applying for grants; they should apply to foundations known for longer-term grants; and they should create plans that justify long-term support from foundations.

Capital Financing↗