Portal vascular route from hypophysial stalk/neural lobe to adenohypophysis

1980 ◽  
Vol 239 (5) ◽  
pp. R463-R469 ◽  
Author(s):  
A. J. Baertschi

Adenohypophysis, neural lobe, stalk, and median eminence are interconnected by capillary networks and portal vessels, but the directions of blood flow are not clearly understood. To test the hypothesis that peptides released from the hypothalamohypophysial tract (HHT) may reach the adenohypophysis, the HHT of anesthetized rats were stimulated electrically with 5-s trains of constant current (400 microA) biphasic impulses (0.2-1 ms) at 30 Hz, and extracellular potassium activity was recorded in various parts of the hypothalamohypophysial complex with microelectrodes (2- to 4-micrometer tip). Within HHT and neural lobe, K+ increased without delay (within 30 ms) from 2.20 +/- 0.25 (meq/l, mean +/- SE) and 2.65 +/- 0.40 to 4.50 +/- 0.60 and 7.60 +/- 0.85, respectively. Within the anterior dorsal regions of the adenohypophysis (AAH), K+ increased from 3.00 +/- 0.25 to 5.05 +/- 0.35, but with a delay of 1-4 s. Within the posterior regions of the dorsal adenohypophysis, the increase was barely significant (P < 0.1) and was delayed by 4-10 s. K+ responses in AAH to nicotine and HHT stimulation were abolished by circulatory arrest; thus K+ responses were not due to current spread or passive diffusion. Coagulation of long portal vessels did not diminish K+ responses in AHH. Results suggest that peptides released from HHT are not only secreted into the general circulation, but may reach the adenohypophysis through a portal vascular route.

1990 ◽  
Vol 258 (5) ◽  
pp. R1242-R1249
Author(s):  
R. B. Page ◽  
M. Gropper ◽  
E. Woodard ◽  
J. Townsend ◽  
S. Davis ◽  
...  

Blood flow was measured in the ovine median eminence and neural lobe before and after the intravenous infusion of dopamine (n = 7), the D1 agonist SKF 38393 (n = 4), the D2 agonist bromocriptine (n = 4), and the dopamine antagonist haloperidol (n = 5). It was also measured before and after the intracarotid infusion of dopamine into eight naive sheep and seven sheep pretreated with phenoxybenzamine. Radiolabeled microspheres were used to determine regional cerebral and regional neurohypophysial blood flows (RNHBF) in these 35 adult female sheep anesthetized with pentobarbital sodium. Samples for serum prolactin measurement by radioimmunoassay were obtained before and after drug infusion. Intravenous dopamine infusion did not change median eminence or neural lobe blood flow (RNHBF) but increased renal and choroid plexus blood flow. Intravenous haloperidol caused a significant fall in RNHBF and blood flow in choroid plexus, caudate nucleus, and kidneys. Intracarotid dopamine infusion decreased RNHBF but increased choroid plexus blood flow. RNHBF was significantly greater in the seven sheep pretreated with phenoxybenzamine than in the eight naive sheep. These findings do not support a role for dopamine in the regulation of median eminence blood flow. The last observation does add support to the hypothesis that norepinephrine or epinephrine interaction with alpha-receptors plays a role in the control of ovine median eminence blood flow and hence in the regulation of delivery of humoral messages from the brain to the anterior pituitary gland.


1981 ◽  
Vol 241 (1) ◽  
pp. R36-R43 ◽  
Author(s):  
R. B. Page ◽  
D. J. Funsch ◽  
R. W. Brennan ◽  
M. J. Hernandez

Regional neurohypophyseal and cerebral blood flows were measured by the radiolabeled microsphere technique in 30 adult sheep under light barbiturate anesthesia. Regional blood flows were determined under basal conditions. The responses of regional blood flow to alterations in arterial PCO2 and to changes in arterial blood pressure wee also determined. In addition, the relationship between regional neurohypophyseal blood flow and neurosecretory activity as judged by plasma arginine vasopressin levels was assessed. Under basal conditions median eminence blood flow averaged 461 ml.100 g-1.min-1 and did not significantly differ from neural lobe blood flow (436 ml.100 g-1.min-1). Blood flow in the neurohypophysis was about 8 times cortical and 16 times white matter blood flow in these animals. Median eminence and neural lobe blood flow proportionately increased far less than regional cortical or white matter blood flow under conditions of hypercarbia. With alteration of arterial blood pressure, regional neurohypophyseal blood flow remained constant beyond the limits of cerebral autoregulation. The neurohypophysis demonstrates a degree of blood flow homeostasis that exceeds that of any other brain area studied. Although the neurohypophysis is a diverticulum of the brain, its vascular system forms a unique functional as well as a unique anatomic unit.


1988 ◽  
Vol 255 (2) ◽  
pp. R295-R302
Author(s):  
R. M. Bryan ◽  
C. L. Myers ◽  
R. B. Page

Regional cerebral blood flow (rCBF) was measured in the neurohypophysis and hypothalamus in normocapnic and hypercapnic rats using [14C]isopropyliodoamphetamine. Rats were surgically prepared using nitrous oxide and halothane and placed in plaster restraining casts. Hypercapnia was produced by increasing the fractional concentration of inspired CO2 (FICO2). rCBF in normocapnic rats was higher in the paraventricular nucleus, supraoptic nucleus, median eminence, and neural lobe than rates previously measured by use of diffusible tracers. During hypercapnia blood flow increased linearly with arterial PCO2 (PACO2) in all regions except the median eminence and neural lobe, which were not affected by hypercapnia. When rats were pretreated with phentolamine (1 mg/kg) to block the alpha-adrenergic receptors, blood flow in the median eminence and neural lobe increased significantly during hypercapnia. We conclude that blood flow in the cell bodies of the paraventricular nucleus and supraoptic nucleus is regulated differently during hypercapnia than blood flow in the nerve terminals in the median eminence and neural lobe. Furthermore, vasodilation produced by increased CO2 is offset by alpha-receptor stimulation in the median eminence and neural lobe.


1984 ◽  
Vol 52 (3) ◽  
pp. 421-434 ◽  
Author(s):  
U. Heinemann ◽  
I. Dietzel

Changes in extracellular K+ concentration [( K+]o) were measured with ion-selective microelectrodes in chronic epileptic foci induced by topical application of A1(OH)3 cream on the sensorimotor cortex of cats. The foci were morphologically characterized by a scar surrounded by an area of marked gliosis. Base-line levels of [K+]o in gliotic tissue and its immediate border zone were comparable to those in normal cortical tissue. Peak levels of [K+]o obtained during repetitive electrical stimulation of the cortical surface and thalamic ventrobasal complex were only slightly enhanced with 11.6 mM in chronic foci and 10.8 mM in normal cortex. Iontophoretic K+ application into gliotic tissue was accompanied by slow negative potential shifts comparable to those observed in normal cortex. Passage of constant current through gliotic tissue caused local [K+]o changes in the vicinity of the current-passing electrode. Since these [K+]o changes were similar to those observed in normal tissue, it was concluded that the amount of transcellularly transported K ions was comparable in both tissues. Changes in the size of extracellular space (ES) were investigated by measuring local concentration changes of iontophoretically injected tetramethylammonium and choline ions. During stimulus-induced seizure activity, the ES shrank outside the gliotic area at sites of maximal [K+]o elevation, while it increased at sites within the gliotic tissue where [K+]o rises were smaller. The results suggest that the spatial buffer capacity of gliotic tissue for K+ is not severely impaired. Since the relationship between rises in [K+]o and subsequent undershoots at sites immediately bordering the gliotic tissue is comparable to that in normal cortex, the ability of this epileptic tissue for active K+ uptake appears to be unaffected. This conclusion is further supported by the observation that iontophoretically induced rises in [K+]o during undershoots are reduced to a similar extent as in normal cortex.


1986 ◽  
Vol 373 (1-2) ◽  
pp. 27-34 ◽  
Author(s):  
D.M. Ziedonis ◽  
W.B. Severs ◽  
R.W. Brennan ◽  
R.B. Page

1993 ◽  
Vol 21 (3) ◽  
pp. 798-808 ◽  
Author(s):  
Robert J. Hariman ◽  
Eric K. Louie ◽  
Rick L. Krahmer ◽  
Siobhan M. Bremner ◽  
David Euler ◽  
...  

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