ABSTRACT

Blood pressure and selected putatively influential hormones were measured in Brattleboro rats which were without diabetes insipidus and which were subjected to various manipulations in dietary sodium intake. Rats fed a control diet from weaning to 16 weeks of age showed a slow increase in blood pressure whereas rats fed a sodium-enriched diet for the same period exhibited sustained hypertension (115±3 versus 169±5 (s.e.m.) mmHg). In animals fed a sodium-enriched diet plasma concentrations of antidiuretic hormone (ADH) were significantly increased from 55±8 to 108±5 fmol/l. Rats fed the control diet from weaning (group A) and subsequently maintained on that diet or changed to a sodium-enriched diet or sodium-deficient diet showed no differences in their blood pressure. Plasma hormone concentrations were similar in these groups, with the exception of aldosterone suppression in rats switched from control to a sodium-enriched diet (0·26±0·04 versus 0·08±0·03 nmol/l; P <0·001). Animals fed the sodium-enriched diet from weaning to 16 weeks of age (group b) and either maintained on that diet or changed to a control diet showed little change in their established hypertension. Transfer to the control diet was associated with increased plasma renin concentrations (PRC) (13·8±2·1 to 122·6±6·2 nmol/l) and plasma aldosterone concentrations (0·04±0·01 to 0·08±0·01 nmol/l; P<0·001) but corticosteroids and ADH concentrations were unchanged. Rats maintained on the sodium-enriched diet from weaning to 16 weeks of age and transfered to a sodium-deficient diet exhibited increases in their established hypertensive blood pressures (maximally 205±4 versus 170±4 mmHg) together with significant increases in PRC (13·8 ±2·1 to 297±79 nmol/l; P< 0·001), aldosterone (0·04±0·01 to 0·23±0·07 nmol/l; P <0·001) and ADH (82·9±15·5 to 466±118 fmol/l; P <0·001), although plasma concentrations of corticosteroids were again unaffected. Thus it would appear that there is a critical developmental stage at which exposure to a sodium-enriched diet subsequently leads to hypertension. Abrupt withdrawal of the sodium-enriched diet produces an exaggerated hypertension involving changes in both ADH and the renin-angiotensin-aldosterone system.

Journal of Endocrinology (1990) 127, 243–248

ABSTRACT

Peripheral plasma concentrations, metabolic clearance rates (MCR) and blood production rates (BPR) of 1α-hydroxycorticosterone (1-OH-B) were determined in female dogfish (Scyliorhinus canicula) under varying environmental conditions. The constant-infusion technique, using high specific activity tritiated 1-OH-B, was applied to measure the MCR, and BPR were derived from the product of plasma concentration and MCR at equilibrium. Urea plasma clearances and apparent BPR were assessed in a similar manner. Fish were adapted stepwise to 140, 120, 90, 80, 70, 60 and 50% normal sea water (about 1000 mosmol/l). In all cases 1-OH-B was the major corticosteroid, cortisol and corticosterone were sought but never detected.

In environments of reduced osmolarity, plasma osmolarity, sodium, chloride and urea concentrations all declined, alongside increases in plasma concentrations, MCR and BPR of 1-OH-B. In fish held in environments at concentrations greater than normal sea water, plasma osmolarity, sodium, chloride and urea concentrations all increased. Plasma clearance of urea increased in fish held in environments more dilute than sea water, while it decreased in the more hyperosmotic waters. It is tentatively concluded that homeostasis of plasma composition, with particular respect to urea, is in part regulated by 1-OH-B in the dogfish.

J. Endocr. (1984) 103, 205–211

ABSTRACT

It is believed that the renin-angiotensin system evolved initially in primitive bony fishes and is absent from elasmobranchs. We have isolated angiotensin I from the incubates of plasma and kidney extracts of an elasmobranch fish, Triakis scyllia, using eel vasopressor activity as an assay system. Its sequence was determined to be H-Asn-Arg-Pro-Tyr-Ile-His-ProPhe-Gln-Leu-OH. Dogfish angiotensin I is teleost-like because of an asparagine residue at position 1 but it is mammalian-like because of an isoleucine residue at position 5. The unique and most important substitution in dogfish angiotensin I is a proline residue at position 3 which may cause significant changes in its tertiary structure. A glutamine residue at position 9 is also unique among all angiotensin Is sequenced to date. Dogfish angiotensin I is more potent than rat angiotensin I in its vasopressor activity in the dogfish but the relationship is reversed in the rat. Thus angiotensin receptors as well as the hormone molecules appear to have evolved during vertebrate phylogeny. Our findings establish the elasmobranch renin-angiotensin system and support the hypothesis that the renin-angiotensin system is a phylogenetically old hormonal system which plays important roles in cardiovascular and fluid homeostasis.

Journal of Endocrinology (1993) 139, 281–285

ABSTRACT

The putative osmoregulatory role of the unique elasmobranch corticosteroid, 1α-hydroxycorticosterone (1α-OH-B), was investigated using dietary protein restriction as a means of limiting urea biosynthetic ability. Groups of dogfish (Scyliorhinus canicula) were adapted to either a high or a low protein diet (HPD and LPD respectively) and the secretory dynamics of urea and 1α-OH-B were determined following acclimation to normal (100%), 130% and 50% sea water.

In normal sea water, LPD fish showed significantly decreased blood production of urea compared with fish fed a HPD (P <0·05), and the plasma urea concentration required to maintain iso-osmolality was achieved only by a substantial decrease in urea clearance from the plasma. Unlike HPD fish, LPD fish in 130% sea water had no apparent ability to increase plasma urea concentration. An alternative strategy adopted by these animals was the retention of high plasma concentrations of Na⁺ and Cl⁻, which increased plasma osmolality and tended to decrease osmotic water loss. Concomitant with the increased ion concentrations, plasma 1α-OH-B concentration was also greatly elevated in LPD fish indicating that the steroid may be acting to minimize Na⁺ (and Cl⁻) excretion at osmoregulatory sites such as the rectal gland, kidney and gills.

This and a previous study have also demonstrated that 1α-OH-B concentration is elevated in 50% sea water. Decreases in plasma Na⁺ concentration are tolerated down to 75% sea water, whereafter Na⁺ is preferentially retained and further decreases in osmolality are achieved by reductions in plasma urea concentration. Increased 1α-OH-B concentration in 50% sea water corresponds to Na⁺ retention and regulation around a lower set point.

The results of this study are consistent with a mineralocorticoid role for 1α-OH-B in elasmobranchs, with 1α-OH-B acting preferentially to maintain plasma Na⁺ concentrations under certain osmotic conditions.

Journal of Endocrinology (1993) 138, 275–282

Arterial rings were prepared from the branchial artery, coeliac artery and ventral aorta of the Japanese dogfish Triakis scyllia and used to determine arterial contraction in a myograph. Noradrenaline caused a dose-dependent contraction (10(-9)-3 x 10(-6) M) that was completely inhibited by pre-treatment with 10(-7) M phentolamine. Homologous dogfish angiotensin II (ANG II) ([Asn1, Pro3, Ile5]-ANG II) also caused dose-dependent contraction (10(-9)-3 x 10(-6) M), but phentolamine had no effect on this response. Administration of dogfish angiotensin I (ANG-I) ([Asn1, Pro3, Ile5, Gln9]-ANG I) resulted in a contraction similar to that produced by ANG II and the effect could be blocked with 10(-7) M captopril. The mammalian ANG II receptor antagonists [Sar1, Ile8]-ANG II and [Sar1, Ala8]-ANG II caused dose-dependent contractions of coeliac artery rings, but were less potent than homologous ANG I and ANG II. These results show that the contractile effect of [Asn1, Pro3, Ile5]-ANG II is not mediated by the alpha-adrenergic system and contractions of arterial rings by noradrenaline and elasmobranch ANG II are mediated by separate vascular receptors. The elasmobranch ANG II vascular receptor may have co-evolved with the unusual structure of this peptide.

ABSTRACT

The effects of an elasmbranch cardiac C-type natriuretic peptide (dogfish CNP-22) on arterial blood pressure were investigated in vivo in chronically cannulated dogfish Scyliorhinus canicula and in vitro by a myographic technique using the distal part of the first branchial artery. In-vivo dogfish CNP-22 caused a dose-dependent reduction in mean arterial blood pressure which was much more potent than that of α-human ANP. In-vitro dogfish CNP-22 also caused a dose-dependent relaxation which was independent of the endothelium. These results are in marked contrast to those obtained in similar studies on other vertebrate species in which CNP exhibited only mild hypotensive effects compared to both atrial and brain natriuretic peptides. This study indicates the importance of using homologous peptides in determing the physiological role of natriuretic peptides in non-mammalian vertebrates.