The effect of intravenous injection of epinephrine on blood volume, red cell volume, and hematocrit was studied. The effects of such a challenge on anesthetized intact, awake intact, and awake splenectomized rats were compared.The epinephrine challenge caused significant increases in the hematocrits of anesthetized animals and highly significant increases in the awake intact animals. No other statistically significant changes occurred in the parameters studied.The results indicate that the rat sequesters red blood cells in the spleen which are released with an appropriate challenge. This release response is attenuated by sodium pentobarbital anesthesia. It was not possible to detect an increase in blood volume or in red cell volume by using Cr51 tagged cells as tracers.Ball State UniversityMuncie, IN 47306

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Thesis (M.S. in Modeling, Virtual Environments, and Simulation)--Naval Postgraduate School, September 2002. / Thesis advisor(s): Russell D. Shilling, Rudolph P. Darken. Includes bibliographical references (p. 55-59). Also available online.

Made available in DSpace on 2015-06-17T19:34:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-09-30. Added 1 bitstream(s) on 2015-06-18T12:47:23Z : No. of bitstreams: 1 000827131_20160930.pdf: 1032389 bytes, checksum: 1ec652e603aca7989376c865a7b92ae6 (MD5) Bitstreams deleted on 2016-10-03T12:15:51Z: 000827131_20160930.pdf,. Added 1 bitstream(s) on 2016-10-03T12:16:37Z : No. of bitstreams: 1 000827131.pdf: 2564151 bytes, checksum: 723e8967f02bfb11f977abb54f8c05f4 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Programa de Doutorado Sanduíche no Exterior (PDSE) / O epidídimo é o órgão do sistema reprodutor masculino responsável pela maturação e armazenamento dos espermatozóides. A contração da cauda do epidídimo (CE) é um dos primeiros eventos da fase de emissão seminal da ejaculação e o sistema nervoso autônomo simpático desempenha um papel importante na contração da CE através da ativação de adrenoceptores α1 (α1-ARs). Neste estudo mostramos que a CE expressa α1A-ARs e α1D-ARs e que ambos os receptores contribuem, de um modo complexo, para a contração da CE induzida por agonistas α1. Na ausência de ativação por agonistas o α1D-ARs modula a contração induzida pela ativação de α1A-ARs por agonistas exógenos. Os α1A-ARs da CE não são dessensibilizados pela oximetazolina. Os andrógenos desempenham um papel importante na manutenção da interação entre os α1A/1D-ARs visto que a redução de andrógenos, mas não de estrógenos, pela castração evidencia a presença dos α1D-ARs. A interação complexa entre os 1A/α1D-ARs é discutida no contexto de heterodimerização de receptores visto que mostramos, pela primeira vez, a heterodimerização entre os α1A e α1D-ARs recombinantes humanos / The epididymis is the male reproductive organ responsible for sperm maturation and storage. The contraction of cauda epididymis (CE) during ejaculation is one of the first events of seminal emission phase of ejaculation and the sympathetic nervous system plays a key role in the CE contraction via α1 adrenoceptors (α1-ARs) activation. In this study we show that CE expresses α1A and α1D-ARs and both receptor subtypes contribute in a complex way to the CE contraction induced by α1-ARs agonists. The α1D modulates α1A-ARs induced contraction irrespective of agonist-mediated α1D activation. There is no desensitization of CE α1A-ARs to oxymetazoline. The androgens were shown to play an important role in the maintenance of such α1A/α1D interaction as the androgen deprivation unravels the cryptic functional α1D-ARs. Estrogens had no effect on α1-ARs mediated contraction of CE. The complex α1A/α1D interaction is discussed in the context of receptor heterodimerization as we showed, for the first time, heteromerization of recombinant α1A/α1D-ARs / Programa de Doutorado Sanduíche no Exterior (PDSE): 12355/13-5

Orientador: Luiz Ricardo de Almeida Kiguti / Coorientador: André Sampaio Pupo / Banca: Edson Antunes / Banca: Sandra Cordellini / Banca: Erick José Ramo da Silva / Resumo: O epidídimo é o órgão do sistema reprodutor masculino responsável pela maturação e armazenamento dos espermatozóides. A contração da cauda do epidídimo (CE) é um dos primeiros eventos da fase de emissão seminal da ejaculação e o sistema nervoso autônomo simpático desempenha um papel importante na contração da CE através da ativação de adrenoceptores α1 (α1-ARs). Neste estudo mostramos que a CE expressa α1A-ARs e α1D-ARs e que ambos os receptores contribuem, de um modo complexo, para a contração da CE induzida por agonistas α1. Na ausência de ativação por agonistas o α1D-ARs modula a contração induzida pela ativação de α1A-ARs por agonistas exógenos. Os α1A-ARs da CE não são dessensibilizados pela oximetazolina. Os andrógenos desempenham um papel importante na manutenção da interação entre os α1A/1D-ARs visto que a redução de andrógenos, mas não de estrógenos, pela castração evidencia a presença dos α1D-ARs. A interação complexa entre os 1A/α1D-ARs é discutida no contexto de heterodimerização de receptores visto que mostramos, pela primeira vez, a heterodimerização entre os α1A e α1D-ARs recombinantes humanos / Abstract: The epididymis is the male reproductive organ responsible for sperm maturation and storage. The contraction of cauda epididymis (CE) during ejaculation is one of the first events of seminal emission phase of ejaculation and the sympathetic nervous system plays a key role in the CE contraction via α1 adrenoceptors (α1-ARs) activation. In this study we show that CE expresses α1A and α1D-ARs and both receptor subtypes contribute in a complex way to the CE contraction induced by α1-ARs agonists. The α1D modulates α1A-ARs induced contraction irrespective of agonist-mediated α1D activation. There is no desensitization of CE α1A-ARs to oxymetazoline. The androgens were shown to play an important role in the maintenance of such α1A/α1D interaction as the androgen deprivation unravels the cryptic functional α1D-ARs. Estrogens had no effect on α1-ARs mediated contraction of CE. The complex α1A/α1D interaction is discussed in the context of receptor heterodimerization as we showed, for the first time, heteromerization of recombinant α1A/α1D-ARs / Doutor

The extreme elevation in plasma levels of norepinephrine (NE) and epinephrine (EP) which occurs during forced diving of ducks (Anas platyrhynchos) was studied before and after denervation of the adrenal glands. Elevated PaCO₂, decreased arterial pH, decreased blood glucose as well as low PaO₂ have been described as causal factors in this response. These variables, as well as blood pressure, heart rate and breathing frequency were measured in ducks dived after breathing air or pure 0₂ to clarify and quantify the mechanism involved and its physiological function. Both NE and EP concentration increased by up to 2 orders of magnitude in the 4 minute dive period, but by a significantly lesser amount if the duck breathed 0₂, before the dive. While pH and PaCO₂ were well correlated with the changes in plasma NE and EP levels during both air and 0₂ dives, both pH and PaCO₂ changed more in the 0₂ trials, indicating that they are not the primary cause of the response. Plasma glucose levels were variable. PaO₂ values less than normal correlated well with increasing NE and EP concentrations, but at high PaO₂s, there was no correlation, suggesting that hypoxia is the permissive state for the full response. Compared with breathing air, breathing O₂ before the dive attenuated the diving bradycardia, eliminated the decrease in blood pressure normally observed during dives, and caused more extreme changes in pH, PaC0₂, and of course, PaO₂. Denervating the adrenals decreased the amounts of both catecholamines released during dives after breathing air and 0₂, EP significantly more than NE. Adrenal denervation per se did not cause a significant change in heart rate, blood pressure, arterial gas tensions, pH, or plasma glucose changes during dives although the operation caused increased variation in some of the parameters. In ducks, the cause for the catecholamine release is decreasing PaO₂ and full expression of the response is dependent on intact innervation of the adrenal gland, although there is a component that is unaffected by denervation. While possible roles for this response are discussed, the true physiological function of this response remains cast in shadows. / Science, Faculty of / Zoology, Department of / Graduate

The cAMP-second messenger hypothesis for β-adrenoceptor-induced relaxation of uterine smooth muscle was tested in high-K+ depolarized rat uterus. At 10⁻⁸ M concentration, Isoproterenol, a β -adrenergic agonist, could cause relaxation of the depolarized uterus without Increasing tissue cAMP levels. Further, although increases in cAMP levels were associated, in some cases, with -isoproterenol (10⁻⁸ M or 10⁻⁴ M)-Induced relaxation, there was no quantitative correlation between the Increases in cAMP and relaxation. Pretreatment of the tissue with a phosphodiesterase Inhibitor, RO 20-1724 (10⁻⁴ M), did not potentiate the relaxation response to Isoproterenol. These results suggested that there Is no simple cause and effect relationship between β -adrenoceptor-Induced Increases in cAMP levels and relaxation in uterine smooth muscle. The dissociation between cAMP and relaxation found ln the present study was also extended to cGMP, since no changes in cGMP levels were observed with isoproterenol-induced relaxation. It is generally accepted that the ionic environment of the cell affects the cellular responses of the tissue. It was demonstrated that hlgh-K*" depolarization of uterine smooth muscle caused an impairment of the ability of isoproterenol to induce cAMP accumulation. This was found to be related to Increased Ca++-Influx known to occur during depolarization. This Is because pretreatment of the tissue with 10⁻⁵M D-600, an Inhibitor of Ca++-lnflux, restored the stimulation of cAMP by Isoproterenol ln the depolarized muscle to a level similar to that observed ln non-depolarized muscle. Furthermore, there was an Inverse relationship between [ca++] ex in the depolarizing medium (range 0.9 to 7.2 mM) and increases in cAMP produced by isoproterenol (10⁻⁴ M). It was also found that exposure of the rat uterus to a Ca++-deficient solution (Ca++-free with 0.2 mM EGTA) accentuated the Increase of tissue cAMP content produced by isoproterenol (10⁻⁸ M). The studies on ionic interactions demonstrated that the presence of Na+(80 mM) or high Mg++(2.5 mM) in the depolarizing medium could overcome the blockade of lsoproterenol-induced increases in cAMP levels by high-K+ depolarization. The studies on the mechanism of this effect of Na+ on the cAMP response revealed that Na+ exerted this effect probably by reducing the Increase In Ca++-influx occurring during depolarization. A similar type of interaction between Mg++ and Ca++ was also observed. These studies have pointed out a possible regulatory role of Ca++ in isoproterenol-lnduced Increases in cAMP levels in uterine smooth muscle. Since it was also demonstrated that cAMP Is not an obligatory requirement In order for Isoproterenol to produce relaxation, these data have raised the question as to whether the Increases ln cAMP produced by β-adrenoceptor stimulation Is an event secondary to the changes in Ca++ movements produced by the agonist. The electrophysiological studies showed that isoproterenol (10 M) could inhibit spontaneous contractility of the rat uterus without causing hyperpolarlzation. In hlgh-K+ depolarized muscle, Isoproterenol (10⁻⁶M) produced relaxation without any change in membrane potential. These data suggested that hyperpolarlzation of cell membranes is not a prerequisite for β-adrenoceptor-med-lated relaxation of uterine smooth muscle. / Pharmaceutical Sciences, Faculty of / Graduate

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

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In the present study alpha-receptor modulation of coronary flow and cardiac function was examined in exercising dogs, chronically instrumented to measure: circumflex blood flow velocity (CFV), heart rate (HR), global left ventricular function (LVP and dP/dt Max) and regional left ventricular function (%SL and dL/dt (s)max). During exercise, local adrenergic blockade was produced by intracoronary injection of 1.0 mg phentolamine ( anon-specific alpha-antagonist) or .5 mp prazosin. Exercise significantly increased HR, LVP, dP/dt max, CFV, %SL and dL/dt (s)max. Neither alpha-antagonist produced changes in HR, LVP or %SL; however, both phentolamine and prazosin produced significant increses in dP/dtmax, CFV and dL/dt(s)max of the alpha-blocked region, when compared to their exercise level before alpha-blockade. It is suggested that an alpha1-adrenergic vasoconstriction limits coronary vasodilation and, thereby, cardiac function during exercise.