Functional connectivity network between terrestrial and aquatic habitats by a generalist waterbird, and implications for biovectoring.

Birds are vectors of dispersal of propagules of plants and other organisms including pathogens, as well as nutrients and contaminants. Thus, through their movements they create functional connectivity between habitat patches. Most studies on connectivity provided by animals to date have focused on movements within similar habitat types. However, some waterbirds regularly switch between terrestrial, coastal and freshwater habitats throughout their daily routines. Lesser black-backed gulls that overwinter in Andalusia use different habitat types for roosting and foraging. In order to reveal their potential role in biovectoring among habitats, we created an inter-habitat connectivity network based on GPS tracking data. We applied connectivity measures by considering frequently visited sites as nodes, and flights as links, to determine the strength of connections in the network between habitats, and identify functional units where connections are more likely to happen. We acquired data for 42 tagged individuals (from five breeding colonies), and identified 5676 direct flights that connected 37 nodes. These 37 sites were classified into seven habitat types: reservoirs, natural lakes, ports, coastal marshes, fish ponds, rubbish dumps and ricefields. The Doñana ricefields acted as the central node in the network based on centrality measures. Furthermore, during the first half of winter when rice was harvested, ricefields were the most important habitat type in terms of total time spent. Overall, 90% of all direct flights between nodes were between rubbish dumps (for foraging) and roosts in other habitats, thereby connecting terrestrial and various wetland habitats. The strength of connections decreased between nodes as the distance between them increased, and was concentrated within ten independent spatial and functional units, especially between December and February. The pivotal role for ricefields and rubbish dumps in the network, and their high connectivity with aquatic habitats in general, have important implications for biovectoring into their surroundings.

Diagnosis of rotator cuff lesions: comparison of US and MRI on 38 joint specimens.

An experimental study was performed on cadaveric joint specimens of the shoulder to determine the accuracy of US and MRI in diagnosis of abnormalities of the rotator cuff. The value of different morphological criteria was evaluated for discrimination of degeneration as well as partial and complete disruption. A total of 38 surgically exposed specimens of the shoulder joint were examined by US, MRI and pathological methods visualising the tendons of the rotator cuff in same axial and longitudinal orientations. The three imaging modalities were reviewed separately by experienced examiners, respectively, who were blind to other results. Evaluation criteria consisted of signs of shape (thinning, thickening, discontinuity and absence of rotator cuff) and structure (changes in echogenicity in US, increased signal intensity in MRI, tissue changes in pathology). Findings in US and MRI were finally compared with pathology to assess sensitivity and specificity. Pathology demonstrated 4 full-thickness tears, 6 partial-thickness tears, 16 cases with degeneration and 12 normal rotator cuffs. Ultrasound showed pathological signs in all abnormal cuffs, and one MRI report was false negative. Specificity was 67 % in US (4 of 12 cases were false positive) and 100 % in MRI (no abnormal findings in healthy tendons). Discrimination of different pathological disorders of the rotator cuff was reduced in both methods. Using US only 10 of 16 cases of degeneration, 2 of 6 partial tears and 3 of 4 complete tears were correctly defined. Using MRI 13 of 16 degenerations, 3 of 6 partial tears and 3 of 4 complete tears were detected. The MRI technique failed to visualise intratendinous calcifications in all 3 cases. We conclude that MRI and US are both sensitive in detection of abnormalities of the rotator cuff. Ultrasound should be the primary diagnostic method in screening of shoulder pain because it is economic and fast. The MRI technique should be used secondary because it provides more information about extent of tendons and has lower risk of artefacts.

Effects of prolonged vasopressin treatment in Brattleboro rats with diabetes insipidus.

Normal Long-Evans rats (LE) exhibited diurnal variations of plasma arginine vasopressin (AVP) concentrations with peak values at 10 A.M. and minimum values at 1 P.M. Brattleboro rats heterozygous for hypothalamic diabetes insipidus (DI) had significantly reduced plasma AVP concentrations and increased plasma osmolalities when compared with LE rats. By prolonged injection of 100 mU/day of vasopressin tannate (VPT) into Brattleboro rats homozygous for DI, plasma AVP concentrations close to those of LE rats were achieved. Potassium was retained for 7 days until escape of vasopressin-induced potassium retention occurred. When 500 mU VPT were injected into DI rats, high plasma AVP levels were induced. Potassium was retained for 2-3 days. After initial sodium retention, periods of natriuresis occurred. During treatment with 100 mU VPT/day most of the alterations present in DI rats were corrected, which included increased water turnover and external water loss, increased hematocrit and plasma sodium concentrations (but not increased plasma osmolalities), hypokalemia, increased activity of the renin-angiotensin system, and reduced adrenocortical function.

Plasma vasopressin concentrations and effects of vasopressin antiserum on blood pressure in rats with malignant two-kidney Goldblatt hypertension.

Male Sprague-Dawley rats with unilateral renal artery stenosis and a contralateral untouched kidney develop a malignant hypertension (MH) which is characterized by high blood pressures, sodium and water depletion, and subsequent activation of the renin-angiotensin system. In the present studies we found plasma arginine vasopressin (AVP) concentrations-3-fold higher than those in rats with benign renal hypertension, and 4- to 5-fold higher than those in normotensive control rats. Analysis of individual values showed considerable scatter; about 50% of the values fell in the range of benign hypertensive or control rats. When a specific AVP antiserum was injected, iv, into eight conscious unrestrained MH rats, BP transiently fell toward control values in four; in one, BP fell by only 10 mm Hg, and three other MH rats showed no response. In the same rats, injection of a specific angiotensin II antiserum always induced a transient fall in BP. On the basis of these and previously reported observations, we conclude that, subsequent to sodium and water loss and activation of the renin-angiotensin system, vasopressin release is stimulated in a significant number of MH rats and that, in these rats, vasopressin may cause significant systemic vasoconstriction. Thereby vasopressin may contribute to the development of malignant renal hypertension in rats.

Comparative study on development of corticosterone and DOCA hypertension in rats.

The administration of corticosterone for 5 consecutive days to normal rats on a standard sodium intake induced negative sodium and water balance. These effects were opposite those observed under DOCA treatment. However, not only under DOCA but also under corticosterone treatment extracellular fluid volume (ECFV) and plasma volume (PV) increased, and blood pressure (BP) rose in parallel. Plasma renin and angiotensin II concentrations declined under the influence of both steroids. Plasma arginine vasopressin concentrations increased under DOCA, whereas they transiently decreased under corticosterone administration. These data suggest that the common mediator for BP elevation due to steroid excess would be an increase in ECFV and PV. The pathways by which this increase is achieved seem to be different. Under DOCA treatment ECFV and PV increased subsequent to renal sodium and water retention. Under corticosterone, however, sodium and water were shifted from intra- to extracellular compartments, and a fraction of this shifted sodium and water was conserved in extracellular space, most likely because corticosterone also affected renal sodium handling.

Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension.

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.

Vasopressin and malignant deoxycorticosterone hypertension in rats.

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin-angiotensin system plays in the pathogenesis of malignant renal hypertension.

Effects of saline drinking on malignant course of renal hypertension in rats.

In rats with unilateral renal artery stenosis and an intact contralateral kidney, a malignant course of hypertension (MH) may develop, which is characterized by 1) high BP levels, 2) sodium and water loss and a polyuric-polydipsic syndrome, 3) marked activation of the renin-angiotensin system, 4) malignant nephrosclerosis in the contralateral kidney and high plasma urea concentrations, and 5) deterioration of the animals' general condition. (Some rats exhibit signs of a cerebral vascular crisis; some rats die). When such rats are offered in addition to water 0.9% NaCl, they compulsively drink the saline, BP falls for some days to levels found in the other hypertensive animals, and signs of MH nearly or completely disappear. It is concluded that high saline intake has, for a limited period, a beneficial effect on the malignant course of renal hypertension in rats. The observations made are consistent with the hypothesis that salt and water loss, which ensue subsequent to an increase of BP into a critical high range might trigger the onset of malignant hypertension.

Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats?

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.

Salt and water balance and renin activity in renal hypertension of rats.

In male Sprague-Dawley rats, renal artery constriction in the presence of an inact contralateral kidney induced sodium retention (for 2-3 wk), moderate potassium loss,elevation of blood volume (BV), and an increase in water turnover. It is suggestedthat renal artery constriction activates the renin-angiotensin-aldosterone system, resulting in disordered regulation of salt and water balance and in blood pressure (BP) elevation. Subsequently, sodium balance was reestablished in one group of hypertensive rats. The previously retained sodium was kept in the body, and BV and reninactivity remained elevated. In a second group of animals, a malignant course of hypertension developed: BP surpassed a critical level of about 180 mmHg; sodium, potassium, and water were lost; BV declined; renin activity was further stimulated; and in the contralateral kidney malignant nephrosclerosis occurred. It is assumed that pressure diuresis and natriuresis induce a vicious circle: the increasing renin activity may maintain or further increase BP level, therby inducing further salt and water loss, etc.; high BP levels and high renin activities induce vascular damage and deterioration of renal function.

Salt appetite during the early phase of renal hypertension in rats.

In male Sprague-Dawley rats the left renal artery was constricted by a 0.2mm silver clip while the contralateral kidney was left untouched. 10 days after clipping the animals were offered, in addition to water, 0.9% saline as drinking fluid for 6 days. Hypertensive animals drank twice as much saline as did control rats throughout the period of observation. In the hypertensive animals, 24-hrs saline intake during the first day of the self-selection study was quantitatively related to the actual height of blood pressure and to the preceding blood pressure increase. After 6 days on the self-selection regimen, plasma angiotensin II concentrations in the hypertensive rats were elevated by 50% when compared with control rats. On the basis of these and previously reported findings (i.e. an increased activity of the renin-angiotensin-aldosterone system and sodium retention) it is suggested: a) despite sodium retention salt appetite is enhanced, indicating a disordered regulation of sodium balance during the early phase of renal hypertension in rats; b) elevated plasma concentrations of angiotensin II and aldosterone could have enhanced salt appetite; c) despite greater salt intake than in control rats the activity of the renin-angiotensin system remains elevated in renal hypertensive rats, thereby possibly inducing a sustained high saline intake.