Comparative effects of catecholamines, angiotensin II and antidiuretic hormone on chloride transport in toad skin

In this work we present data which show stimulation of Cl- transport in the isolated toad skin by four agonists: L-isoproterenol, L-adrenalin, angiotensin II and ADH. This response was demonstrated by raising mucosal amiloride concentration to block the sodium transport in the skin. With transepithelial sodium influx almost completely inhibited, it was likely that the response reflected transport events in the glands. Inhibition of the bioelectric parameters by removing chloride from the serosal bathing medium in the amiloride-inhibited preparation eliminated the response to all four agents, indicating that these responses are chloride dependent. The similarity of the bioelectric responses of the amiloride-treated preparation to db cAMP and to the four agents tested in this work add further evidence that this second messenger may account largely for the Cl- transport mechanism in the toad skin glands by increasing the apical membrane permeability to Cl-.     

Influence of season on plasma antidiuretic hormone, angiotensin II, aldosterone and plasma renin activity in young volunteers

We investigated seasonal changes in hormonal and thermoregulatory responses. Eight volunteers were subjected to the experiment at four times of the year: around the vernal and autumnal equinoxes, and at the summer and winter solstices at latitude 35° N. Plasma antidiuretic hormone (ADH), angiotensin II (ANG II), aldosterone (ALD) and plasma renin activity (PRA) were analyzed before and after water immersion. Seasonal changes in thermoregulatory responses were assessed by measuring core temperature and sweat rate during immersion of the leg in hot water (at 42°C) for 30 min in a room maintained at 26°C. The concentration of plasma ADH and ALD before water immersion was significantly higher in summer than in other seasons. The concentrations of ANG II and PRA did not show seasonal variations. Changes in tympanic temperature during water immersion showed significant differences between seasons, and were higher in winter than in other seasons. The sweat rate was significantly higher in summer than in other seasons. In summary, ADH and ALD concentrations displayed a seasonal rhythm with marked elevation in summer; this may be a compensative mechanism to prevent dehydration from increased sweat loss during summer due to heat acclimatization.     

Dehydration and fluid balance: central effects of angiotensin

Central effects of dehydration are stimulated by osmotic stimuli, the reduced input of volume receptors, and angiotensin II. The subfornical organ (SFO) and organum vasculosum laminae terminalis (OVLT) have become accepted as putative receptor sites for angiotensin II in the brain. The exact quantitative relationship between the hours of water deprivation and the amount of angiotensin generated peripherally and whether that amount is sufficient to induce thirst centrally have not been established, but there is no question that when animals are dehydrated their angiotensin levels rise and the animals are thirsty. Attempts to block centrally the contribution of angiotensin II to thirst have been variable and cholinergic inputs have to be blocked at the same time. Various stimuli for thirst interact in a parallel fashion, and when one stimulus is blocked the other stimuli are still effective. Plasma angiotensin II may induce natural thirst, but how it enters the brain still remains to be explained. Although the SFO and OVLT have no blood-brain barrier, the blood supply to these organs acts as a limited perfusion system whereby blood-borne proteins cannot diffuse far from the capillary bed. A second set of receptors is found on the ventricular surface of the OVLT, as shown by fluorescence labeled angiotensin II. The connection between the SFO and OVLT was cut by discrete knife cuts. Drinking to angiotensin II intraventricularly was not significantly altered but the pressor response was reduced by 50%. These results can be explained by a circuit for drinking passing down below the level of the knife cut and a separate pressor pathway passing dorsally through the area that was cut by the knife. Thirst and pressor neural circuits beginning with angiotensin receptors could explain some of the data accumulated with the AV3V syndrome that occurs when the OVLT and nucleus medianas are destroyed.     

Interactions of gonadotropin-releasing hormone (GnRH) and gonadotropin-inhibitory hormone (GnIH) in birds and mammals

Gonadotropin-releasing hormone (GnRH) regulates secretion of both of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone. Thus, it is a key hormone for vertebrate reproduction. GnRH was considered to be unusual among hypothalamic neuropeptides in that it appeared to have no direct antagonist, although some neurochemicals and peripheral hormones (opiates, GABA, gonadal steroids, inhibin) can modulate gonadotropin release to a degree. Five years ago, a vertebrate hypothalamic neuropeptide that inhibited pituitary gonadotropin release in a dose-dependent manner was discovered in quail by Tsutsui et al. (2000. Biochem Biophys Res Commun 275:661-667). We now know that this inhibitory peptide, named gonadotropin-inhibitory hormone, or GnIH, is a regulator of gonadotropin release in vitro and in vivo. Its discovery has opened the door to an entirely new line of research within the realm of reproductive biology. In our collaborative studies, we have begun to elucidate the manner in which GnIH interacts with GnRH to time release of gonadotropins and thus time reproductive activity in birds and mammals. This paper reviews the distribution of GnIH in songbirds relative to GnRHs, and our findings on its modes of action in vitro and in vivo, based on laboratory and field studies. These data are simultaneously compared with our findings in mammals, highlighting how the use of different model species within different vertebrate classes can be a useful approach to identify the conserved actions of this novel neuropeptide, along with its potential importance to vertebrate reproduction.     

Role of prostaglandins in the mediation of systemic tachyphylaxis to angiotensin II

Angiotensin-induced prostaglandin release has been implicated in the development of tachyphylaxis to angiotensin $\text{in vitro}$. Based on these findings and evidence that prostaglandins modulate the angiotensin response locally, experiments were done to investigate the role of prostaglandins in the systemic tachyphylaxis to angiotensin. Rats were given intravenous infusions of 1-asparaginyl-5-valyl and 1-aspartyl-5-isoleucyl angiotensin II at two different doses. Using systemic blood pressure as a parameter, varying degrees of tachyphylaxis were produced and the aspartyl analog was found to be more tachyphylactic. When rats were given indomethacin, a prostaglandin synthesis inhibitor, the response to intravenous infusion of aspartyl angiotensin was not significantly altered.     

Regulation of angiotensin II receptors in cultured rat ovarian granulosa cells by follicle-stimulating hormone and angiotensin II

The regulation of ovarian granulosa cell angiotensin II (Ang-II) receptor formation and progesterone secretion by follicle-stimulating hormone (FSH) and Ang-II was studied in cultured cells prepared from hypophysectomized, diethylstilbestrol-treated immature rats. Ang-II receptors (estimated by the specific cell binding of the Ang-II receptor antagonist 125I-[Sar1,Ile8]Ang-II) were present on freshly prepared granulosa cells and increased by over 2-fold (to 2150 binding sites/cell; KD = 0.5 nM) when cultured in serum-free medium for 48 h. FSH prevented the normal increase in Ang-II receptor expression. Maximal FSH-dependent decrease in Ang-II receptors and increase in progesterone secretion occurred at 100 ng/ml FSH. The inhibitory effect of FSH on granulosa cell Ang-II receptor content was partially mimicked by the cAMP analogue 8-bromo-cAMP, since 8-bromo-cAMP suppressed (by 96%) Ang-II receptor content to a greater extent than FSH (by 60%). Granulosa cell Ang-II receptor content was not modified by progesterone or 17 beta-estradiol, but was decreased by testosterone (by 35%). Ang-II also produced a decrease in granulosa cell Ang-II receptor content, but did not modify progesterone secretion or aromatase activity. The effect of Ang-II on granulosa cell Ang-II receptor content was mimicked by the Ca2+ ionophore A23187, but not by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate, suggesting that an elevation of cytosolic Ca2+ may be important for the homologous down-regulation of the Ang-II receptor. These data show homologous and heterologous down-regulation of granulosa cell Ang-II receptors. If these regulatory mechanisms exist in the FSH-sensitive healthy follicle, our findings suggest that in the process of maturation, healthy and dominant follicles may become decoupled from angiotensinergic influences.     

Role of angiotensin II and corticotropin-releasing hormone in hemodynamic responses to cocaine and stress

Cocaine produces characteristic behavioral and autonomic responses due to its unique pharmacological properties. Many of the autonomic responses resemble those to acute behavioral stress. Both cocaine and behavioral stress have been shown to evoke an increase in sympathetic nerve activity that is primarily responsible for the peripheral cardiovascular responses. We noted varying hemodynamic and sympathetic response patterns to cocaine administration and to acute behavioral stress in rats that correlate with the predisposition to develop both a sustained increase in arterial pressure and cardiomyopathies. Several lines of evidence suggest that the autonomic response patterns are dependent on the actions of central peptides including angiotensin II (Ang II) and corticotropin-releasing hormone (CRH). This is based on observations demonstrating that intracerebroventricular (icv) administration of receptor antagonists for Ang II or CRH attenuated the decrease in cardiac output (CO) and increase in vascular resistance noted in some animals after cocaine administration or startle. In contrast, icv Ang II enhances the cardiodepression associated with cocaine administration or startle. Based on this and other evidence, we propose that the autonomic response patterns to startle and to cocaine are closely related and dependent on central Ang II and CRH. Furthermore, we suggest that these central peptides may be responsible for varying predisposition to cardiovascular disease.     

Effect of recombinant human growth hormone on urinary 15N-nitrogen balance in girls with Turner syndrome as compared to children with growth hormone deficiency

15N-nitrogen balances before and on human growth hormone (hGH) were studied in 13 girls with Turner syndrome (TS) aged 4.4-16 (median 13.2) years (45,X0 or equivalent, no X0/XX mosaicism, no estrogen replacement). The results were compared with those reported from 9 patients with growth hormone deficiency (GHD). The TS patients received subcutaneous hGH doses of 2 x 3 (group A, n = 6), 3 x 2 (group B, n = 3), or 2 x 6 (group C, n = 4) IU/m2 on consecutive days. The mean 15N dose given to the patients of groups A and C was higher (13.6 mg/kg) than that given to those of group B (2.7 mg/kg). The lower hGH doses in the first two groups induced small positive mean 15N balance changes (+0.6 +/- 0.6 mg/kg 15N, group A; +0.03 mg/kg, group B). The higher hGH dose in group C caused a more marked mean balance change (+3.0 mg/kg 15N) comparable to that in GHD patients (+3.2 mg/kg). Individual variation of response, however, was larger in patients with TS than in those with GHD. With low and high hGH doses, there were responders and nonresponders. It is concluded from this pilot study in a small number of cases that 15N balance studies might be potentially useful to choose the appropriate hGH dose for long-term treatment in TS patients.     

Development of the clavicles in birds and mammals

Clavicles (collar bones) are variably present in mammals. Furculae (wishbones)--which may or may not be homologous with clavicles--are variably present and/or fused in birds and present in theropod dinosaurs. In this overview the development of clavicles and furculae is discussed with special attention to modes of skeletogenesis (whether intramembranous or endochondral), numbers of centres of ossification (one in chick furculae; two in murine clavicles), presence of cartilage (primary in clavicles, secondary in furculae), evidence from experimental analysis and from mutations for dependence of both clavicular and furcular growth on mechanical stimulation, and syndromes and mutations affecting clavicular development leading to both under and over development. J. Exp. Zool. 289:153-161, 2001.     

Noradrenaline as a possible mediator of angiotensin II induced fluid transport in rat ileum in vitro

In isolated segments of ileum excised from bilaterally adrenalectomized and nephrectomized rats, 10(-12) M angiotensin or 10(-3) M noradrenaline added to serosal medium stimulated both fluid transfer and NaCl transport. The alpha adrenergic antagonist phentolamine blocked the stimulation of fluid transfer induced by angiotensin. These results are consistent with the hypothesis that noradrenaline may mediate the increase of intestinal fluid absorption induced by angiotensin in the rat. In segments of isolated ileum from normal rats 10(-12) M angiotensin only stimulated fluid transfer under one of the two following conditions when 10(-3) M imipramine, a noradrenaline uptake blocker, was present in the serosal medium; or when the rats had been previously treated with L-Dopa, a precursor of noradrenaline biosynthesis. These results suggested that the necessity for bilateral adrenalectomy and nephrectomy might be associated to the necessity of increasing the tissue levels of noradrenaline. Direct measurement of noradrenaline tissue content confirmed this.     

Prolactin as a regulator of fluid and electrolyte metabolism in mammals

The evidence that prolactin is a fluid and electrolyte regulator in mammals is reviewed, with particular emphasis on the renal actions of prolactin. Prolactin receptors are found in mammalian kidneys. Prolactin modulates renal formation of cyclic AMP and polyamines and it leads to demonstrable histological changes in the proximal tubules. The renal actions of prolactin primarily involve modulation of the effects of other hormones and are therefore critically dependent on the background physiological situation. Prolactin seems able to cause a prolonged reduction in water, sodium, and potassium excretion, a pattern that is imitated by no other hormone with the possible exception of growth hormone. Prolactin preparations can cause an acute antidiuresis, which may in part be related to contamination of prolactin preparations with vasopressin. However, most of the described effects cannot be explained by vasopressin contamination. This is particularly so with the effects of prolactin on water movements across fetal skin, the amniotic membrane, and in the eye where prolactin and vasopressin have diametrically opposite effects. It is concluded that prolactin is a regulator of fluid and electrolyte metabolism in mammals but that it is a modulator rather than a primary controlling factor.     

Particularities of reproduction and oogenesis in teleost fish compared to mammals

Compared to mammals, teleost reproduction presents many original features. Reproductive strategies of species are diversified into numerous adaptations to a large variety of aquatic environments. This diversity may concern sexuality, spawning and parental behaviour, sensitivity to environmental factors, and specific features of gametogenesis such as the duration of vitellogenesis, and egg morphology. Sexuality presents a variety of natural modalities, from gonochorism to hermaphrodism. The absence of definitive arrest of body growth in the adult of most species gives a particular interest to the practical control of growth-reproduction interactions. Vitellogenesis, which represents an important metabolic effort for the maternal organism, involves the synthesis of vitellogenin, a specific glycolipo-phosphoprotein produced in the liver under estradiol stimulation, and its incorporation into oocytes by a receptor mediated process. Both estradiol synthesis in follicle cells and vtg uptake by vitellogenic follicles appear to be mainly controlled by FSH. Oocyte maturation is directly triggered by a progestin, or MIS (maturation inducing steroid) synthesised in follicle cells mainly under LH control, and acting through the non-genomic activation of a membrane receptor. Practical applications of some of these particularities result mainly from the external character of the fertilisation process and of embryonic development, which allows manipulating respectively egg chromosome stocks and sex differentiation. Moreover, the sensitivity of sex differentiation to exogenous factors favours the development of practical methods to control the sex of farmed populations. Finally, the sensitivity of reproductive mechanisms to xenobiotics has led to various kinds of bioassays for putative pollutants.     

Structure of the cardiac systole in mammals and birds

The comparative analysis of the contractile function of the heart left ventricle in four species of homoeothermic tetrapods (chicken, quail, rat, sheep) who differ in their spatio-temporal pattern of ventricular excitation, heart rate, and heart weight was performed. The analysis of cardiac cycle structure was performed on the basis of synchronous recording of ECG, phonocardiogram, and apex cardiogram. Indices of myocardial contractility of the left ventricle calculated on the basis of the analysis of the cardiac dynamics indicate disadvantageous contractile function of the left ventricle in rodents and non-flying birds in comparison with sheep. The functioning of the left ventricle in male rats is more strained than in female rats. One fundamental factor determining a more strained functioning of the left ventricle in birds in comparison with mammals is the heart rate. The relative weight and activation pattern of the left ventricular myocardium govern the contractile function of the left ventricle to a lesser extent.     

Central hypertensive actions of angiotensin I, II and III in conscious rats

The effects of intracerebroventricular administrations of three natural angiotensins, angiotensin I (ANG I 3.8 X 10-11-9.4 X10-10 mol/kg body weight), II (9.6 X 10-12-2.4 X 10-10 mol/kg body weight) and III (2.7 X 10-10 2.5 X 10-9 mol/kg body weight) on systemic blood pressure were investigated in conscious rats. Angiotensin II (ANG II), ANG I and angiotensin III (ANG III), increased blood pressure in a dose-related manner. The order of potency of angiotensins was ANG II greater than ANG I greater than ANG III. The intraventricular administration of a converting enzyme inhibitor (SQ 14225, 6.9 X10-8 mol/kg) abolished the central effect of ANG I, while an angiotensin II analogue ([Sar1-Ala8]ANG II, 1.1 X 10-8 mol/kg) administered intraventricularly inhibited the central pressor effects of these three angiotensins. These results suggest that ANG II is a main mediator of the renin-angiotensin system in the central nervous system.