scholarly journals Tyrosine hydroxylase immunoreactivity as indicator of sympathetic activity: simultaneous evaluation in different tissues of hypertensive rats

2011 ◽  
Vol 300 (2) ◽  
pp. R264-R271 ◽  
Author(s):  
Katia Burgi ◽  
Marina T. Cavalleri ◽  
Adilson S. Alves ◽  
Luiz R. G. Britto ◽  
Vagner R. Antunes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Tyrosine Hydroxylase ◽  
Sympathetic Activity ◽  
High Performance ◽  
Hypertensive Rats ◽  
Regional Patterns ◽  
Spontaneously Hypertensive ◽  
Direct Recording ◽  
Wistar Kyoto ◽  
Different Tissues

Vasomotor control by the sympathetic nervous system presents substantial heterogeneity within different tissues, providing appropriate homeostatic responses to maintain basal/stimulated cardiovascular function both at normal and pathological conditions. The availability of a reproducible technique for simultaneous measurement of sympathetic drive to different tissues is of great interest to uncover regional patterns of sympathetic nerve activity (SNA). We propose the association of tyrosine hydroxylase immunoreactivity (THir) with image analysis to quantify norepinephrine (NE) content within nerve terminals in arteries/arterioles as a good index for regional sympathetic outflow. THir was measured in fixed arterioles of kidney, heart, and skeletal muscle of Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (123 ± 2 and 181 ± 4 mmHg, 300 ± 8 and 352 ± 8 beats/min, respectively). There was a differential THir distribution in both groups: higher THir was observed in the kidney and skeletal muscle (∼3–4-fold vs. heart arterioles) of WKY; in SHR, THir was increased in the kidney and heart (2.4- and 5.3-fold vs. WKY, respectively) with no change in the skeletal muscle arterioles. Observed THir changes were confirmed by either: 1) determination of NE content (high-performance liquid chromatography) in fresh tissues (SHR vs. WKY): +34% and +17% in kidney and heart, respectively, with no change in the skeletal muscle; 2) direct recording of renal (RSNA) and lumbar SNA (LSNA) in anesthetized rats, showing increased RSNA but unchanged LSNA in SHR vs. WKY. THir in skeletal muscle arterioles, NE content in femoral artery, and LSNA were simultaneously reduced by exercise training in the WKY group. Results indicate that THir is a valuable technique to simultaneously evaluate regional patterns of sympathetic activity.

Peripheral and Central Catecholaminergic Neurons in Genetic and Experimental Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 377s-380s ◽  
Author(s):  
H. Grobecker ◽  
J. M. Saavedra ◽  
M. F. Roizen ◽  
V. Weise ◽  
I. J. Kopin ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Adrenal Glands ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Hydroxylase Activity ◽  
Methyl Transferase ◽  
Spontaneously Hypertensive ◽  
Catecholaminergic Neurons ◽  
Wistar Kyoto ◽  
The Brain

1. Activity of peripheral and central catecholaminergic neurons was studied in spontaneously hypertensive rats (SHR) and deoxycorticosterone (DOCA)—salt hypertensive rats. 2. In young SHR (4 weeks) the plasma values of both noradrenaline and dopamine-β-hydroxylase activity were increased compared with those of normotensive rats of the Wistar/Kyoto strain. Total catecholamines (mostly adrenaline) were not significantly different. 3. In the adrenal glands of 2-weeks-old and 4-weeks-old SHR activities of tyrosine hydroxylase, dopamine-β-hydroxylase, phenylethanolamine-N-methyl transferase were decreased, compared to Wistar/Kyoto rats. 4. The adrenaline-forming enzyme was elevated in the A1 and A2 regions of the brain stem of 4-weeks-old SHR and in the A1 region of adult DOCA—salt hypertensive rats. 5. In the adrenal glands of adult DOCA—salt hypertensive rats tyrosine hydroxylase activity was increased. 6. These results implicate peripheral noradrenaline-containing neurons and central adrenaline-containing neurons in the development of genetic and experimental hypertension in rats.

Pathways of bradykinin degradation in blood and plasma of normotensive and hypertensive rats

2001 ◽  
Vol 280 (5) ◽  
pp. H2182-H2188 ◽  
Author(s):  
Andreas Dendorfer ◽  
Sebastian Wolfrum ◽  
Marc Wagemann ◽  
Fatimunnisa Qadri ◽  
Peter Dominiak
Keyword(s):  
High Performance ◽  
Enzymatic Degradation ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive ◽  
Angiotensin I Converting Enzyme ◽  
Aminopeptidase P ◽  
Carboxypeptidase N ◽  
Wistar Kyoto

Kinins are vasoactive peptide hormones that can confer protection against the development of hypertension. Because their efficacy is greatly influenced by the rate of enzymatic degradation, the activities of various kininases in plasma and blood of spontaneously hypertensive rats (SHR) were compared with those in normotensive Wistar-Kyoto rats (WKY) to identify pathogenic alterations. Either plasma or whole blood was incubated with bradykinin (10 μM). Bradykinin and kinin metabolites were measured by high-performance liquid chromatography. Kininase activities were determined by cumulative inhibition of angiotensin I-converting enzyme (ACE), carboxypeptidase N (CPN), and aminopeptidase P (APP), using selective inhibitors. Plasma of WKY rats degraded bradykinin at a rate of 13.3 ± 0.94 μmol · min−1· l−1. The enzymes ACE, APP, and CPN represented 92% of this kininase activity, with relative contributions of 52, 25, and 16%, respectively. Inclusion of blood cells at physiological concentrations did not extend the activities of these plasma kininases further. No differences of kinin degradation were found between WKY and SHR. The identical conditions of kinin degradation in WKY and SHR suggest no pathogenic role of kininases in the SHR model of genetic hypertension.

Diminished sympathetic silent period in spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. R147-R152 ◽  
Author(s):  
L. P. Schramm ◽  
G. N. Barton
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Silent Period ◽  
Spontaneous Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Splanchnic Nerves ◽  
Wistar Kyoto ◽  
Stimulation Of

To determine if elevated sympathetic activity occurs in spontaneously hypertension, the silent period induced in splanchnic nerves following electrical stimulation of dorsal medullary sympathoexcitatory sites was compared in anesthetized normotensive Wistar Kyoto rats (WKYs) and Okamoto spontaneously hypertensive rats (SHRs). The strength of silent periods was defined as the degree of inhibition of responses to testing stimuli delivered at various latencies following conditioning trains, and it was assumed to be inversely related to the level of sympathetic activity. Weanling SHRs exhibited weaker silent periods than weanling WKYs although, at that age, the arterial pressures of the strains were not significantly different. Silent periods were also weaker in adult SHRs than in adult WKYs. This difference persisted after arterial pressures, which fell under anesthesia, were raised by phenylephrine infusions to the respective "normal" levels in each strain. These results support the hypothesis that elevated sympathetic activity exists during both the development and maintenance of spontaneous hypertension in rats.

Effects of dietary sodium on central and peripheral ouabain-like activity in spontaneously hypertensive rats

1993 ◽  
Vol 264 (6) ◽  
pp. H2051-H2055 ◽  
Author(s):  
F. H. Leenen ◽  
E. Harmsen ◽  
H. Yu ◽  
C. Ou
Keyword(s):  
Left Ventricle ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Dietary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
Later Phase ◽  
Shr And Wky Rats

High dietary Na+ intake enhances pressor and sympathoexcitatory responses in spontaneously hypertensive rats (SHR) but not Wistar-Kyoto (WKY) rats. To evaluate the possible contribution of central ouabain-like activity (OLA), brain and peripheral OLA was assessed in SHR vs. WKY rats at 4 wk of age and after 2 and 4 wk of high vs. control Na+ intake started at 4 wk of age. In SHR, hypertension developed with maturation and was exacerbated by high Na+ intake. With control Na+ intake, SHR showed higher OLA at 4, 6, and 8 wk of age in the pituitary and hypothalamus and also by 8 wk in the adrenals and left ventricle but not in plasma. High Na+ intake increased OLA in all tissues examined in both WKY rats and SHR. After 2 wk on high Na+, only OLA in hypothalamus and pituitary was higher in SHR vs. WKY rats; after 4 wk on high Na+, peripheral (i.e., adrenals, left ventricle, and plasma) OLA was also higher. These results indicate that in SHR the development of hypertension is associated early on with increases in central OLA and in a later phase with increases in peripheral OLA as well. High Na+ intake increases OLA in both SHR and WKY rats, but the higher OLA may affect sympathetic activity and blood pressure only in SHR.

Sympathetic activity in spontaneously hypertensive rats after spinal transection

1982 ◽  
Vol 243 (5) ◽  
pp. R506-R511 ◽  
Author(s):  
L. P. Schramm ◽  
E. S. Chornoboy
Keyword(s):  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Spontaneously Hypertensive ◽  
Sympathetic Hyperactivity ◽  
Ganglionic Blockade ◽  
Renal Nerve Activity ◽  
Wistar Kyoto

To test the hypothesis that sympathetic hyperactivity and hyperexcitability in spontaneously hypertensive rats (SHR) is generated at spinal and/or ganglionic levels, we measured integrated renal nerve activity (before ganglionic blockade) and adrenal nerve activity (after ganglionic blockade) in 12- to 14-wk-old SHR and normotensive Wistar-Kyoto rats (WKY). Rats were anesthetized with alpha-chloralose, artificially respired, and paralyzed. Spinal cords were transected at C1 to eliminate normal supraspinal control of sympathetic activity. The effectiveness of descending sympathoexcitatory and sympathoinhibitory pathways was tested by measuring changes in nerve activity elicited by graded spinal stimulation. Spontaneous renal nerve activity was elevated in SHR, but stimulation of descending excitatory pathways caused similar responses in SHR and WKY. Spontaneous adrenal preganglionic nerve activity was similar in SHR and WKY, but excitatory stimulation elicited larger adrenal nerve responses in SHR. We conclude that spinal and/or ganglionic mechanisms may generate a component of the sympathetic hyperactivity exhibited by SHR. The larger adrenal preganglionic nerve responses to excitatory stimulation in SHR suggest that spinal systems may be partially responsible for adrenomedullary hyperexcitability in spontaneous hypertension.

Altered carnitine metabolism in spontaneously hypertensive rats

1985 ◽  
Vol 249 (2) ◽  
pp. E183-E186 ◽  
Author(s):  
K. A. Foster ◽  
B. O'Rourke ◽  
D. K. Reibel
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Spontaneously Hypertensive Rats ◽  
Elevated Serum ◽  
Total Serum ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Fatty Acid Utilization ◽  
Carnitine Metabolism ◽  
Wistar Kyoto

Carnitine metabolism was examined in spontaneously hypertensive rats (SHR). Carnitine levels were elevated by 25% in hypertrophied hearts of 10- and 15-wk-old SHR when compared with Wistar-Kyoto (WKy) controls. This elevation was associated with a greater than 25% increase in total serum carnitine. The elevated serum carnitine does not appear to be due to increased mobilization from skeletal muscle because carnitine levels were elevated by 25% in gastrocnemius and diaphragm of SHR. Elevated serum carnitine is also not a result of reduced urinary excretion because daily urinary carnitine output was increased by 150% in SHR. These findings suggest that the most likely mechanism for increased serum carnitine is increased carnitine synthesis by the liver. The changes in carnitine metabolism in SHR appear to occur between 5 and 10 wk of age, because the carnitine levels in serum and organs were comparable in 5-wk-old WKy and SHR. The observed alterations in tissue and serum carnitine levels may result in altered fatty acid utilization in SHR.

Enhanced Sympathetic Activity Caused by Salt Loading in Spontaneously Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 171s-173s ◽  
Author(s):  
R. Dietz ◽  
A. Schoumig ◽  
W. Rascher ◽  
R. Strasser ◽  
W. Kubler
Keyword(s):  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Plasma Adrenaline ◽  
Spontaneously Hypertensive ◽  
Noradrenaline Concentration ◽  
Wistar Kyoto ◽  
Distinct Increase ◽  
Stimulation Of

1. Salt loading accelerates and increases the rise in blood pressure (spSH) in stroke-prone spontaneously hypertensive rats, but not in Wistar-Kyoto (WK) rats. 2. In both strains a slight increase in plasma volume was obtained during salt loading. 3. Salt loading caused a distinct increase in plasma noradrenaline concentration in spSH rats, but a slight decrease in WK rats. Plasma adrenaline and dopamine concentrations remained unaffected. 4. Exposure to cold resulted in a more marked stimulation of sympathoadrenal and sympathoneuronal activity in salt-loaded spSH rats than in spSH rats on a normal sodium diet. 5. It is concluded that salt loading results in a further increase of the already elevated sympathetic activity in spSH rats.

Angiotensin II in neuronal cultures from brains of normotensive and hypertensive rats

1984 ◽  
Vol 247 (1) ◽  
pp. C115-C119 ◽  
Author(s):  
M. K. Raizada ◽  
B. Stenstrom ◽  
M. I. Phillips ◽  
C. Sumners
Keyword(s):  
Angiotensin Ii ◽  
High Performance ◽  
De Novo ◽  
Neuronal Cultures ◽  
Ang Ii ◽  
De Novo Synthesis ◽  
Hypertensive Rats ◽  
Primary Neuronal Cultures ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Primary neuronal cultures from 1-day-old rat brains, which contain angiotensin II (ANG II) immunoreactivity within the neurons and are capable of de novo synthesis of this immunoreactivity, have been used in this study to determine the nature of this immunoreactivity by high-performance liquid chromatography (HPLC). Neuronal cultures from the brains of normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SH) rats were found to contain ANG II immunoreactivity, which co-migrated with authentic ANG II on HPLC. The angiotensin detected in brain cultures was not derived from the growth medium, and its level was significantly decreased by incubating the cultures with captopril. A 71% decrease in the levels of ANG II was observed in neuronal cultures of SH rat brains compared with those from WKY controls. These observations show that differences in brain angiotensin between SH and WKY are present before differences in blood pressure are manifested.

Na+/H+ and HCO3−/Cl− exchange in the control of intracellular pH in vivo in the spontaneously hypertensive rat

1991 ◽  
Vol 81 (6) ◽  
pp. 743-750 ◽  
Author(s):  
P. D. Syme ◽  
J. K. Aronson ◽  
C. H. Thompson ◽  
E. M. Williams ◽  
Y. Green ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Ph ◽  
Acid Concentration ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Concentration Changes ◽  
Wistar Kyoto

1. We have previously shown that the cytosolic acid concentration changes in skeletal muscle during contraction in spontaneously hypertensive rats and normotensive Wistar-Kyoto rats in vivo. We have now found that this change was unaffected by 20% inhaled CO2 or by 4,4′-di-isothiocyanostilbene-2,2′-disulphonate. This is evidence that HCO3− exchange in vivo is not important in the control of cytosolic acid concentration during skeletal muscle contraction in either spontaneously hypertensive or Wistar-Kyoto rats. 2. We have also previously shown that the difference in cytosolic acid response during contraction between spontaneously hypertensive and Wistar-Kyoto rats is due to increased Na+/H+ antiporter activity in the spontaneously hypertensive rats. Our current findings suggest that this increase in Na+/H+ antiporter activity is more likely to be due to a change in the Km of the antiporter than to a change in the Vmax. We estimate that the Km of the antiporter changes in hypertension from pH 7.16 to 7.33. 3. We did not find any differences between adult spontaneously hypertensive and Wistar-Kyoto rats with regard to resting intracellular and extracellular pH and resting intracellular and extracellular HCO3− concentrations. In addition, we did not find any evidence of a difference in skeletal muscle HCO3−/Cl− exchange between adult spontaneously hypertensive and Wistar-Kyoto rats. 4. At rest, skeletal muscles of the spontaneously hypertensive and Wistar-Kyoto rats have the same lactate production, HCO3−/Cl− exchange and arterial partial pressure of CO2. In addition, we can also calculate that at a resting intracellular pH of 7.05 in the spontaneously hypertensive rats, the antiporter is 66% saturated. The corresponding value in the Wistar-Kyoto rats (resting intracellular pH 7.04) is 57%. This explains the lack of difference in resting intracellular pH between the two strains of rat and suggests that at rest differences in Na+/H+ antiporter activity due to a shift in Km of the antiporter are too small to result in a difference in resting pH. 5. Furthermore, Na+/H+ antiporter activity around pH 7.0 was unable to prevent the acidosis caused by CO2 loading. Thus resting pH in skeletal muscle in vivo is determined largely by the HCO3− system and in this regard skeletal muscle is similar to vascular smooth muscle.

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