Renal nerve inhibition by central NaCl and ANG II is abolished by lesions of the lamina terminalis

2000 ◽  
Vol 279 (5) ◽  
pp. R1827-R1833 ◽  
Author(s):  
C. N. May ◽  
R. M. McAllen ◽  
M. J. McKinley
Keyword(s):  
Hypertonic Saline ◽  
Third Ventricle ◽  
Plasma Renin ◽  
Anterior Wall ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Renal Nerve ◽  
Intracerebroventricular Infusion ◽  
Conscious Sheep ◽  
Nerve Inhibition

The lamina terminalis is situated in the anterior wall of the third ventricle and plays a major role in fluid and electrolyte homeostasis and cardiovascular regulation. The present study examined whether the effects of intracerebroventricular infusion of hypertonic saline and ANG II on renal sympathetic nerve activity (RSNA) were mediated by the lamina terminalis. In control, conscious sheep ( n = 5), intracerebroventricular infusions of 0.6 M NaCl (1 ml/h for 20 min) and ANG II (10 nmol/h for 30 min) increased mean arterial pressure (MAP) by 6 ± 1 ( P < 0.001) and 14 ± 3 mmHg ( P < 0.001) and inhibited RSNA by 80 ± 6 ( P < 0.001) and 89 ± 7% ( P < 0.001), respectively. Both treatments reduced plasma renin concentration (PRC). Intracerebroventricular infusion of artificial cerebrospinal fluid (1 ml/h for 30 min) had no effect. In conscious sheep with lesions of the lamina terminalis ( n = 6), all of the responses to intracerebroventricular hypertonic saline and ANG II were abolished. In conclusion, the effects of intracerebroventricular hypertonic saline and ANG II on RSNA, PRC, and MAP depend on the integrity of the lamina terminalis, indicating that this site plays an essential role in coordinating the homeostatic responses to changes in brain Na+ concentration.

Brain angiotensinergic pathways mediate renal nerve inhibition by central hypertonic NaCl in conscious sheep

1997 ◽  
Vol 272 (2) ◽  
pp. R593-R600 ◽  
Author(s):  
C. N. May ◽  
R. M. McAllen
Keyword(s):  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Chloride Concentration ◽  
Plasma Renin ◽  
Renal Nerve ◽  
Intracerebroventricular Infusion ◽  
Conscious Sheep ◽  
Renal Sympathetic

The renal sympathetic responses to infusion of hypertonic solutions into the lateral cerebral ventricles were investigated in conscious sheep. Intracerebroventricular infusion of artificial cerebrospinal fluid (CSF) containing 0.6 M NaCl, at 1 ml/h for 20 min, reduced renal sympathetic nerve activity (RSNA) by 81 +/- 5% (n = 6, P < 0.001). Plasma renin concentration also fell (P < 0.05), whereas arterial pressure increased by 6.4 +/- 0.7 mmHg (P < 0.01). Intracerebroventricular hypertonic sorbitol (0.9 M in CSF at 1 ml/h) had no effect. The AT1 receptor antagonist losartan (1 mg/h) abolished the plasma renin and arterial pressure responses to intracerebroventricular hypertonic saline and significantly reduced the fall in RSNA to 17 +/- 10% (P < 0.001). During intracerebroventricular hypertonic saline, the baroreflex relation of RSNA to diastolic pressure was shifted to the left and that to central venous pressure was abolished compared with control relations obtained by manipulating pressure with intravenous phenylephrine. These findings indicate that 1) RSNA is inhibited by a central mechanism that senses high sodium (or perhaps chloride) concentration rather than hypertonicity; 2) this inhibition occurs independently of reflexes from high- and low-pressure baroreceptors, although these may enhance the inhibition; and 3) inhibition of RSNA by hypertonic saline involves a central angiotensinergic pathway.

Baroreceptor-independent renal nerve inhibition by intracerebroventricular angiotensin II in conscious sheep

1997 ◽  
Vol 273 (2) ◽  
pp. R560-R567 ◽  
Author(s):  
C. N. May ◽  
R. M. McAllen
Keyword(s):  
Angiotensin Ii ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Ang Ii ◽  
Central Administration ◽  
Renal Nerve ◽  
Intracerebroventricular Infusion ◽  
Conscious Sheep ◽  
Nerve Inhibition ◽  
Relationship Of

The effect of central administration of angiotensin II (ANG II) on efferent renal sympathetic nerve activity (RSNA) was studied in conscious sheep. ANG II (1 nmol/h), infused for 30 min into the lateral cerebral ventricles in five sheep, did not alter mean arterial pressure (MAP) but reduced RSNA to 38 +/- 5% of control. Intracerebroventricular infusion of higher doses of ANG II (3 and 10 nmol/h), which increased MAP by 12 +/- 2 and 14 +/- 3 mmHg, respectively, reduced RSNA to 9 +/- 5 and 11 +/- 7% of control. MAP and RSNA gradually returned to control over a period of 2 h after the infusions. Intracerebroventricular losartan (1 mg/h for 1 h before, and then during, angiotensin infusion) blocked all the effects of angiotensin (3 nmol/h). Baroreflex relationships constructed from the beat-to-beat relationship of RSNA to diastolic pressure showed a significant leftward shift during intracerebroventricular ANG II compared with the control relationship. The beat-to-beat relationship between central venous pressure and RSNA was abolished during intracerebroventricular infusion of ANG II. These findings demonstrate that intracerebroventricular ANG II has a direct central inhibitory action on RSNA that is independent of both arterial and low-pressure baroreceptors. This effect of angiotensin is mediated by central angiotensin AT-1 receptors.

Activation of kidney-directed neurons in the lamina terminalis by alterations in body fluid balance

2001 ◽  
Vol 281 (5) ◽  
pp. R1637-R1646 ◽  
Author(s):  
D. J. Sly ◽  
M. J. McKinley ◽  
B. J. Oldfield
Keyword(s):  
Hypertonic Saline ◽  
Fluid Balance ◽  
Body Fluid ◽  
Water Deprivation ◽  
Pseudorabies Virus ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Fos Protein ◽  
Neural Substrate ◽  
Body Fluid Balance

This study was undertaken to determine if neurons in the lamina terminalis, previously identified as projecting to the kidney (35), were responsive to alterations in stimuli associated with fluid balance homeostasis. Neurons in the lamina terminalis projecting to the kidney were identified by the retrograde transynaptic transport of Bartha's strain of pseudorabies virus in anesthetized rats. Rats were also exposed to 24-h water deprivation, intravenous hypertonic saline, or intracerebroventricular ANG II. To determine if “kidney-directed” neurons were activated following each stimulus, brain sections that included the lamina terminalis were examined immunohistochemically for viral antigen and Fos protein. With the exception of ANG II in the subfornical organ, all regions of the lamina terminalis contained neurons that were significantly activated by water deprivation, hypertonic saline, and ANG II. These results provide evidence for a neural substrate, which may underpin some of the effects of hypertonic saline and ANG II on renal function thought to be mediated through the lamina terminalis.

Central losartan blocks natriuretic, vasopressin, and pressor responses to central hypertonic NaCl in sheep

1998 ◽  
Vol 275 (2) ◽  
pp. R548-R554 ◽  
Author(s):  
Michael L. Mathai ◽  
Mark D. Evered ◽  
Michael J. McKinley
Keyword(s):  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Pressor Response ◽  
Electrolyte Balance ◽  
Neural Pathways ◽  
Intracerebroventricular Administration ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
The Central Nervous System ◽  
Vasopressin Secretion

This study investigated the effect of intracerebroventricular administration of the angiotensin AT1 receptor antagonist losartan on the natriuresis, pressor effect, and arginine vasopressin (AVP) secretion caused by intracerebroventricular infusion of either ANG II, hypertonic saline, or carbachol. Losartan (1 mg/h) or artificial cerebrospinal fluid (CSF) was infused into the lateral ventricle before, during, and after infusions of either ANG II at 10 μg/h for 1 h, 0.75 mol/l NaCl at 50 μl/min for 20 min, or carbachol at 1.66 μg/min for 15 min. Intracerebroventricular infusions of ANG II, 0.75 mol/l NaCl, or carbachol caused increases in renal Na+ and K+ excretion, arterial pressure, and plasma AVP levels. Increases in arterial pressure, Na+ excretion, and plasma AVP concentration ([AVP]) in response to intracerebroventricular ANG II or intracerebroventricular 0.75 mol/l NaCl were either abolished or attenuated by intracerebroventricular infusion of losartan but not by intracerebroventricular infusion of artificial CSF or intravenous losartan. Intracerebroventricular losartan did not reduce the increase in plasma [AVP] or arterial pressure in response to intracerebroventricular carbachol, but it did attenuate the natriuretic response to intracerebroventricular carbachol. We conclude that an intracerebroventricular dose of losartan (1 mg/h) that inhibits responses to intracerebroventricular ANG II also inhibits vasopressin secretion, natriuresis, and the pressor response to intracerebroventricular hypertonic saline. These results suggest that common neural pathways are involved in the responses induced by intracerebroventricular administration of ANG II and intracerebroventricular hypertonic NaCl. We propose that intracerebroventricular infusion of hypertonic saline activates angiotensinergic pathways in the central nervous system subserving the regulation of fluid and electrolyte balance and arterial pressure in sheep.

Investigation of the mechanisms by which chronic infusion of an acutely subpressor dose of angiotensin II induces hypertension

2007 ◽  
Vol 292 (5) ◽  
pp. R1893-R1899 ◽  
Author(s):  
S. G. Hood ◽  
T. Cochrane ◽  
M. J. McKinley ◽  
C. N. May
Keyword(s):  
Angiotensin Ii ◽  
Low Dose ◽  
Control Period ◽  
Indirect Evidence ◽  
Ang Ii ◽  
Peripheral Vasoconstriction ◽  
Blood Flows ◽  
Intracerebroventricular Infusion ◽  
Chronic Infusion ◽  
Conscious Sheep

The mechanisms by which chronic infusion of an initially subpressor low dose of angiotensin II (ANG II) causes a progressive and sustained hypertension remain unclear. In conscious sheep ( n = 6), intravenous infusion of ANG II (2 μg/h) gradually increased mean arterial pressure (MAP) from 82 ± 3 to 96 ± 5 mmHg over 7 days ( P < 0.001). This was accompanied by peripheral vasoconstriction; total peripheral conductance decreased from 44.6 ± 6.4 to 38.2 ± 6.7 ml·min−1·mmHg−1 ( P < 0.001). Cardiac output and heart rate were unchanged. In the regional circulation, mesenteric, renal, and iliac conductances decreased but blood flows were unchanged. There was no coronary vasoconstriction, and coronary blood flow increased. Ganglion blockade (125 mg/h hexamethonium for 4 h) reduced MAP by 13 ± 1 mmHg in the control period and by 7 ± 2 mmHg on day 8 of ANG II treatment. Inhibition of central AT1 receptors by intracerebroventricular infusion of losartan (1 mg/h for 3 h) had no effect on MAP in the control period or after 7 days of ANG II infusion. Pressor responsiveness to incremental doses of intravenous ANG II (5, 10, 20 μg/h, each for 15 min) was unchanged after 7 days of ANG II infusion. ANG II caused no sodium or water retention. In summary, hypertension due to infusion of a low dose of ANG II was accompanied by generalized peripheral vasoconstriction. Indirect evidence suggested that the hypertension was not neurogenic, but measurement of sympathetic nerve activity is required to confirm this conclusion. There was no evidence for a role for central angiotensinergic mechanisms, increased pressor responsiveness to ANG II, or sodium and fluid retention.

Stimulation of cardiac sympathetic nerve activity by central angiotensinergic mechanisms in conscious sheep

2004 ◽  
Vol 286 (6) ◽  
pp. R1051-R1056 ◽  
Author(s):  
Anna M. D. Watson ◽  
Rasim Mogulkoc ◽  
Robin M. McAllen ◽  
Clive N. May
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity ◽  
Conscious Sheep

Central actions of angiotensin play an important role in cardiovascular control and have been implicated in the pathogenesis of hypertension and heart failure. One feature of centrally or peripherally administered angiotensin is that the bradycardia in response to an acute pressor effect is blunted. It is unknown whether after central angiotensin this is due partly to increased cardiac sympathetic nerve activity (CSNA). We recorded CSNA and arterial pressure in conscious sheep, at least 3 days after electrode implantation. The effects of intracerebroventricular infusions of ANG II (3 nmol/h for 30 min) and artificial cerebrospinal fluid (CSF) (1 ml/h) were determined. The response to intracerebroventricular hypertonic saline (0.6 M NaCl in CSF at 1 ml/h) was examined as there is evidence that hypertonic saline acts via angiotensinergic pathways. Intracerebroventricular angiotensin increased CSNA by 23 ± 7% ( P < 0.001) and mean arterial pressure (MAP) by 7.6 ± 1.2 mmHg ( P < 0.001) but did not significantly change heart rate ( n = 5). During intracerebroventricular ANG II the reflex relation between CSNA and diastolic blood pressure was significantly shifted to the right ( P < 0.01). Intracerebroventricular hypertonic saline increased CSNA (+9.4 ± 6.6%, P < 0.05) and MAP but did not alter heart rate. The responses to angiotensin and hypertonic saline were prevented by intracerebroventricular losartan (1 mg/h). In conclusion, in conscious sheep angiotensin acts within the brain to increase CSNA, despite increased MAP. The increase in CSNA may account partly for the lack of bradycardia in response to the increased arterial pressure. The responses to angiotensin and hypertonic saline were losartan sensitive, indicating they were mediated by angiotensin AT-1 receptors.

scholarly journals Modified one-piece extended transbasal approach for translamina terminalis resection of retrochiasmatic third ventricular craniopharyngioma

2013 ◽  
Vol 34 (v1supplement) ◽  
pp. 1 ◽  
Author(s):  
James K. Liu
Keyword(s):  
Skull Base ◽  
Third Ventricle ◽  
Blind Spot ◽  
Anterior Wall ◽  
Anterolateral Approach ◽  
Lamina Terminalis ◽  
Base Approach ◽  
The Third ◽  
Skull Base Approach ◽  
Midline Approach

Retrochiasmatic third ventricular craniopharyngiomas are formidable tumors to remove surgically. Access to the third ventricle can be achieved through the lamina terminalis corridor. A skull base approach to the lamina terminalis can be performed using either an anterolateral approach (orbitozygomatic, pterional, supraorbital) or a midline approach (extended transbasal, subfrontal). The major disadvantage of an anterolateral approach is the lack of visualization of the ipsilateral wall of the third ventricle and hypothalamus. However, a midline transbasal approach eliminates this blind spot thereby providing direct visualization of both ependymal walls for safe dissection of the tumor. In this operative video manuscript, the author demonstrates an illustrative step-by-step technique for translamina terminalis resection of a retrochiasmatic retroinfundibular craniopharyngioma within the third ventricle via a modified one-piece extended transbasal approach. This approach uses the standard bifrontal craniotomy and incorporates the anterior wall of the frontal sinus as a one-piece flap. The inferior limit of the osteotomy is based along the coronal contour of the anterior skull base which eliminates any bony overhang that can obstruct the line of sight to the lamina terminalis. Additional removal of the supraorbital bar is not necessary. The operative technique for this skull base approach and surgical nuances for craniopharyngioma resection are illustrated in this video atlas.The video can be found here: http://youtu.be/E3Bsp6dUdAE.

Comparative actions of adrenomedullin and nitroprusside: interactions with ANG II and norepinephrine

2001 ◽  
Vol 281 (6) ◽  
pp. R1887-R1894 ◽  
Author(s):  
Christopher J. Charles ◽  
M. Gary Nicholls ◽  
Miriam T. Rademaker ◽  
A. Mark Richards
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Urine Flow ◽  
Plasma Aldosterone ◽  
Ang Ii ◽  
Biological Responses ◽  
Conscious Sheep

The role of adrenomedullin (ADM) in volume and pressure homeostasis remains undefined. Accordingly, we compared the biological responses to infusions of ADM and nitroprusside (NP; matched for reduction of arterial pressure) and assessed their effects on responses to ANG II and norepinephrine in eight conscious sheep. During matched falls in arterial pressure (8–10 mmHg, both P < 0.001) ADM and NP induced similar increases in heart rate. ADM increased cardiac output ( P < 0.001), and the fall in calculated peripheral resistance was greater with ADM than NP ( P = 0.013). ADM infusions raised plasma ADM levels ( P < 0.001), plasma renin activity ( P = 0.001), and ANG II ( P < 0.001) but tended to blunt any concurrent rise in aldosterone compared with NP ( P = 0.056). ADM maintained both urine flow ( P < 0.001) and sodium excretion ( P = 0.01) compared with falls observed with NP. ADM attenuated the vasopressor actions of exogenous ANG II ( P = 0.006) but not norepinephrine. In addition, ADM antagonized the ANG II-induced rise in plasma aldosterone ( P < 0.001). In conclusion, ADM induces a different spectrum of hemodynamic, renal, and endocrine actions to NP. These results clarify mechanisms by which ADM might contribute to volume and pressure homeostasis.

Investigations on the physiological controls of water and saline intake in C57BL/6 mice

2003 ◽  
Vol 285 (2) ◽  
pp. R394-R403 ◽  
Author(s):  
Ralph F. Johnson ◽  
Terry G. Beltz ◽  
Robert L. Thunhorst ◽  
Alan Kim Johnson
Keyword(s):  
Hypertonic Saline ◽  
Neural Control ◽  
Salt Intake ◽  
Third Ventricle ◽  
Salt Appetite ◽  
Ang Ii ◽  
Cellular Dehydration ◽  
Short Period ◽  
Intracerebroventricular Injections ◽  
Ad Libitum

To examine the behavioral and neural control of body fluid homeostasis, water and saline intake of C57BL/6 mice was monitored under ad libitum conditions, after treatments that induce water or salt intake, and after ablation of the periventricular tissue of the anteroventral third ventricle (AV3V). Mice have nocturnal drinking that is most prevalent after the offset and before the onset of lights. When given ad libitum choice, C57BL/6 mice show no preference for saline over water at concentrations up to 0.9% NaCl and a progressive aversion to saline above that concentration. Systemic hypertonic saline, isoproterenol, and polyethylene glycol treatments are dipsogenic; however, systemic ANG II is not. Intracerebroventricular injections of both hypertonic saline and ANG II are dipsogenic, and diuretic treatment followed by a short period of sodium deprivation induces salt intake. After ablation of the AV3V, mice can be nursed to recovery from initial adipsia and, similar to rats, show chronic deficits to dipsogenic treatments. Taken together, the data indicate that mechanisms controlling thirst in response to cellular dehydration in C57BL/6 mice are similar to rats, but there are differences in the efficacy of extracellular dehydration-related mechanisms, especially for systemic ANG II, controlling thirst and salt appetite.

Intravenous hypertonic saline induces Fos immunoreactivity in neurons throughout the lamina terminalis

1991 ◽  
Vol 561 (1) ◽  
pp. 151-156 ◽  
Author(s):  
B.J. Oldfield ◽  
R.J. Bicknell ◽  
R.M. McAllen ◽  
R.S. Weisinger ◽  
M.J. McKinley
Keyword(s):  
Hypertonic Saline ◽  
Lamina Terminalis
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