155
Chapter seven: Water balance
functional response resulting in increased water reabsorption. Fasting induced an increase
in plasma AVP concentration and urine osmolality that were positively correlated, and
decreased urine flow in Baikal and ringed seals (Hong et al. 1982), consistent with AVP function. Furthermore, in the gray seal, fasting increased urine and plasma osmolality along
with an increase in plasma AVP (Skog and Folkow 1994). Collectively these data suggest
that the observed increases in urine osmolality are the result of AVP-mediated increase in
tubular water reabsorption. In the West Indian manatee, a significant correlation between
plasma vasopressin and osmolality was detected further suggesting that the typical regulation of AVP secretion is conserved among these marine mammals (Ortiz et al. 1998).
Conversely, in fasting northern elephant seal pups increasing urine osmolality was
associated with decreasing plasma AVP in the presence of constant plasma osmolality suggesting that increased urine concentration was achieved independent of AVP (Ortiz et al.
1996). Furthermore, in fasting elephant seal pups, an acute bolus infusion of AVP induced
an osmotic diuresis with no change in free water clearance suggesting that acutely elevated AVP does not have a typical mammalian function (Ortiz et al. 2003). However, in
response to an iso- and hyperosmotic saline challenge in fasting elephant seal pups, urinary AVP excretion and free water clearance were inversely correlated (i.e., increased AVP
was correlated with an increase in free water reabsorption) suggesting that under these
stimulatory conditions AVP possesses a typical mammalian function (Ortiz et al. 2002).
Collectively, these data in fasting elephant seal pups suggest that static, chronic measures
of plasma AVP and osmolality are not sufficient indicators of AVP function and that acute
challenges may better elucidate the functionality of AVP in marine mammals.
Additionally, circulating concentrations of AVP often fail to be directly related to
plasma osmolality in cetaceans. AVP is synthesized and secreted into circulation in dolphins as would be expected for any other mammal; however, plasma AVP concentrations
in dolphins are relatively low for mammals (Malvin and Rayner 1968; Malvin et al. 1971;
Ortiz et al. 2000, 2010). Suzuki et al. have also detected a AVP-like molecule by highly sensitive matrix-assisted laser desorption/ionization-time of flight mass spectrometry from
the pituitary of a bottlenose dolphin; however, plasma AVP levels were not correlated with
either plasma or urine osmolality (personal observation). Plasma AVP concentrations were
also not correlated with urine flow in fasting bottlenose dolphins suggesting that AVP
does not significantly contribute to the regulation of water retention (Malvin et al. 1971).
While a postprandial increase in plasma NaCl levels were associated with an increase in
urinary AVP levels suggesting that AVP secretion at least is regulated in a typical manner
(Ballarin et al. 2011), the anti-diuretic function of AVP is still inconclusive in cetaceans.
7.2.5.2 Renin–angiotensin aldosterone system
Renin–angiotensin aldosterone system (RAAS) is important for the control of sodium excretion and blood pressure. As shown in Figure 7.3, renin secretion from the juxta-glomerular
(JG) cells in the kidney is stimulated by renal sympathetic nerve activity in response to
changes in renal arterial pressure or reduced delivery of tubular Na + . Conversely, renin
is suppressed by an increase in tubular Na + delivery to the JG cells. Secreted renin acts
to convert circulating angiotensinogen to angiotensin I, which is subsequently converted to
angiotensin II (Ang II) by the angiotensin-converting enzyme (ACE) (Ichikawa and Harris
1991). In turn, Ang II promotes the secretion of aldosterone from adrenal gland, and aldosterone then stimulates the renal reabsorption of Na + distal tubule and collecting duct
resulting in a decrease in urinary Na + excretion (Funder 1993; Eaton and Pooler 2009).
In marine mammals, RAAS is present and appears to possess a typical mammalian
function. Eichelberger et al. (1940) confirmed the vasoconstrictive action of renin extracted
Chapter seven: Water balance
functional response resulting in increased water reabsorption. Fasting induced an increase
in plasma AVP concentration and urine osmolality that were positively correlated, and
decreased urine flow in Baikal and ringed seals (Hong et al. 1982), consistent with AVP function. Furthermore, in the gray seal, fasting increased urine and plasma osmolality along
with an increase in plasma AVP (Skog and Folkow 1994). Collectively these data suggest
that the observed increases in urine osmolality are the result of AVP-mediated increase in
tubular water reabsorption. In the West Indian manatee, a significant correlation between
plasma vasopressin and osmolality was detected further suggesting that the typical regulation of AVP secretion is conserved among these marine mammals (Ortiz et al. 1998).
Conversely, in fasting northern elephant seal pups increasing urine osmolality was
associated with decreasing plasma AVP in the presence of constant plasma osmolality suggesting that increased urine concentration was achieved independent of AVP (Ortiz et al.
1996). Furthermore, in fasting elephant seal pups, an acute bolus infusion of AVP induced
an osmotic diuresis with no change in free water clearance suggesting that acutely elevated AVP does not have a typical mammalian function (Ortiz et al. 2003). However, in
response to an iso- and hyperosmotic saline challenge in fasting elephant seal pups, urinary AVP excretion and free water clearance were inversely correlated (i.e., increased AVP
was correlated with an increase in free water reabsorption) suggesting that under these
stimulatory conditions AVP possesses a typical mammalian function (Ortiz et al. 2002).
Collectively, these data in fasting elephant seal pups suggest that static, chronic measures
of plasma AVP and osmolality are not sufficient indicators of AVP function and that acute
challenges may better elucidate the functionality of AVP in marine mammals.
Additionally, circulating concentrations of AVP often fail to be directly related to
plasma osmolality in cetaceans. AVP is synthesized and secreted into circulation in dolphins as would be expected for any other mammal; however, plasma AVP concentrations
in dolphins are relatively low for mammals (Malvin and Rayner 1968; Malvin et al. 1971;
Ortiz et al. 2000, 2010). Suzuki et al. have also detected a AVP-like molecule by highly sensitive matrix-assisted laser desorption/ionization-time of flight mass spectrometry from
the pituitary of a bottlenose dolphin; however, plasma AVP levels were not correlated with
either plasma or urine osmolality (personal observation). Plasma AVP concentrations were
also not correlated with urine flow in fasting bottlenose dolphins suggesting that AVP
does not significantly contribute to the regulation of water retention (Malvin et al. 1971).
While a postprandial increase in plasma NaCl levels were associated with an increase in
urinary AVP levels suggesting that AVP secretion at least is regulated in a typical manner
(Ballarin et al. 2011), the anti-diuretic function of AVP is still inconclusive in cetaceans.
7.2.5.2 Renin–angiotensin aldosterone system
Renin–angiotensin aldosterone system (RAAS) is important for the control of sodium excretion and blood pressure. As shown in Figure 7.3, renin secretion from the juxta-glomerular
(JG) cells in the kidney is stimulated by renal sympathetic nerve activity in response to
changes in renal arterial pressure or reduced delivery of tubular Na + . Conversely, renin
is suppressed by an increase in tubular Na + delivery to the JG cells. Secreted renin acts
to convert circulating angiotensinogen to angiotensin I, which is subsequently converted to
angiotensin II (Ang II) by the angiotensin-converting enzyme (ACE) (Ichikawa and Harris
1991). In turn, Ang II promotes the secretion of aldosterone from adrenal gland, and aldosterone then stimulates the renal reabsorption of Na + distal tubule and collecting duct
resulting in a decrease in urinary Na + excretion (Funder 1993; Eaton and Pooler 2009).
In marine mammals, RAAS is present and appears to possess a typical mammalian
function. Eichelberger et al. (1940) confirmed the vasoconstrictive action of renin extracted