Neural and non-neural components of the developing hypertension in genetically hypertensive rats

Kushinsky, Roslyn; Bell, Christopher

doi:10.1016/0165-1838(83)90042-5

Cited by 11 publications

(4 citation statements)

References 16 publications

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“…8 * 14 Also, studies in the GH strain have shown that hypertension can be reversed completely by ganglion blocking agents until the rats are about 4 weeks of age. 15 There are, therefore, several lines of evidence to suggest that elevated sympathetic drive may be an etiologic factor in the genesis of high blood pressure in these animal models for essential hypertension.…”

Section: Neuropeptide Y In Rat Sympathetic Neurons Is Altered By Genementioning

confidence: 99%

Neuropeptide Y in rat sympathetic neurons is altered by genetic hypertension and by age.

et al. 1990

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We have used immunocytochemistry to quantitate neuronai neuropeptide Y in superior cervical ganglia of a strain of nonnotensive Wistar-Otago rats and a related genetically hypertensive strain over the age range 1-60 weeks. The numbers of neuropeptide Y-immunoreactive cells and total ganglionic cell numbers were both greater in ganglia of young nonnotensive than in those of hypertensive rats. Between 10 and 60 weeks of age, peptide immunoreactivity and total cell numbers both fell in nonnotensive rat ganglia but remained constant in ganglia from hypertensive rats. Densitometric analysis showed that the concentrations of neuropeptide Y were similar in neurons of age-matched individuals of both strains, but during aging there was a substantial decline in neuronai peptide content that was similar in both strains and that was not accompanied by any decline in neuronai immunoreactivity for tyrosine hydroxylase. Our results suggest that there is a developmental abnormality of neuropeptide Y in sympathetic neurons of this strain of genetically hypertensive rat and that, furthermore, the aging process is accompanied by a selective loss of neuronai neuropeptide Y that is independent of blood pressure status. (Hypertension 1990;16:63-71) I n adult animals of both the Otago (GH) and the Kyoto (SHR) strains of rat with a hereditary predisposition to hypertension, there is biochemical and functional evidence that peripheral sympathetic activity is inappropriately high.1 -7 Furthermore, neonatal destruction of the peripheral sympathetic nervous system retards the development of hypertension and reduces the absolute extent to which both blood pressure elevation and the associated cardiovascular hypertrophy are seen in adulthood. 8 * 14Also, studies in the GH strain have shown that hypertension can be reversed completely by ganglion blocking agents until the rats are about 4 weeks of age. 15There are, therefore, several lines of evidence to suggest that elevated sympathetic drive may be an etiologic factor in the genesis of high blood pressure in these animal models for essential hypertension. In the sympathetic nervous system, neuropeptide tyrosine or neuropeptide Y (NPY) is jointly localized 23 Therefore, we compared the patterns of NPY immunoreactivity in sympathetic neurons of nonnotensive and GH hypertensive rats from the neonatal period through late adulthood. Methods AnimalsThe rats used in the present study were raised in our animal house from a normotensive white Wistar line originating in the Otago Medical School and from the GH line that was bred from the same stock.24 Breeding was from brother-sister matings, and ah 1 rats were fed a proprietary rat chow (quoted sodium content 0.5%) with water ad libitum. Periodic checks of blood pressures in conscious, prewarmed adult rats using an occlusive tail cuff and a pulse transducer confirmed that resting systolic pressures were less than 140 mm Hg in normotensive rats and at least 170 mm Hg in hypertensive rats.

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Section: Neuropeptide Y In Rat Sympathetic Neurons Is Altered By Genementioning

confidence: 99%

Neuropeptide Y in rat sympathetic neurons is altered by genetic hypertension and by age.

et al. 1990

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“…12 Both male (300-400 g) and female (200-300 g) animals (age, 3-4 months) were used, and the hypertensive and normotensive Wistar rats were age-matched. All rats were fed a proprietary rat chow (quoted sodium content, 0.5%) and given water ad libitum.…”

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Catecholamines in kidneys of normotensive and genetically hypertensive rats. Effects of salt load.

Petrovic¹,

Bell²

1986

Hypertension

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The tissue content of norepinephrine, dopamine, and epinephrine was determined in different zones of the kidney in normotensive Sprague-Dawley and Otago Wistar rats and in genetically hypertensive Otago Wistar rats. One kidney in each animal was chronically denervated to allow estimation of the neuronal contribution to renal catecholamine content. In all strains, the renal cortex contained negligible amounts of nonneuronal norepinephrine and dopamine, while outer and inner medullary layers contained progressively larger amounts. Nonneuronal epinephrine was distributed fairly evenly through cortex and medulla. Neuronal norepinephrine content was similar in inner and outer cortex, substantially less in outer medulla, and not discernible in inner medulla. The amounts of neuronal dopamine were consistent with its localization predominantly in noradrenergic nerves. The renal cortices of normotensive Wistar rats contained more neuronal norepinephrine and less neuronal dopamine than those of Sprague-Dawley rats, and the cortices of hypertensive Wistar rats contained slightly more norepinephrine than those of normotensive Wistar rats. In both normotensive strains, long-term salt loading decreased selectively the neuronal norepinephrine in renal cortex. By contrast, in hypertensive animals, cortical norepinephrine was not reduced by salt loading. These results indicate that the genetically hypertensive rat may have an abnormal sympathetic reflex response to increased blood volume.

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“…In the Otago (GH) strain of hypertensive rat, neonatal destruction of the sympathetic nervous system retards development of high blood pressure (Clark, 1977;Liard, 1977), and, in weanling animals, the hypertension can be reversed completely by ganglionic blockade (Kushinsky and Bell, 1983). Furthermore, adult GH animals do not exhibit the normal withdrawal of renal sympathetic drive that accompanies volume loading (Petrovic and Bell, 1986).…”

Section: Discussionmentioning

confidence: 99%

Quantitation of tyrosine hydroxylase and neuropeptide Y immunoreactivity in single rat sympathetic neurons: Effects of preganglionic nerve activity

Gurusinghe

Harris

Abbott

et al. 1991

J of Neuroscience Research

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Using computerised densitometry to measure immunocytochemical reaction product in a model system, we established conditions that produced a linear relationship between the logarithm of antigen concentration and the measured intensity of staining. We then applied the densitometric technique to assess the changes in tyrosine hydroxylase (TH) and neuropeptide tyrosine (NPY) within sympathetic neurons of rat superior cervical ganglion following chronic decentralization and following reserpine treatment. One week after surgical or pharmacological decentralization, there was appreciable reduction of neuronal levels of both TH and NPY. However, there remained considerable variation in the immunoreactivities of individual cells. Three days of treatment with reserpine elevated TH levels but substantially reduced NPY. Both these effects were prevented by prior decentralization of the ganglia. No differences were seen between normotensive and the Otago strain of genetically hypertensive rats, either in basal TH or NPY immunoreactivities or in responses to the maneuvers performed. Comparison of our findings with previous biochemical data indicate that densitometric immunocytochemistry provides an accurate index of neuronally localised antigen concentrations but also allows analysis of interneuronal differences that are not otherwise apparent.

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Neural and non-neural components of the developing hypertension in genetically hypertensive rats

Cited by 11 publications

References 16 publications

Neuropeptide Y in rat sympathetic neurons is altered by genetic hypertension and by age.

Neuropeptide Y in rat sympathetic neurons is altered by genetic hypertension and by age.

Catecholamines in kidneys of normotensive and genetically hypertensive rats. Effects of salt load.

Quantitation of tyrosine hydroxylase and neuropeptide Y immunoreactivity in single rat sympathetic neurons: Effects of preganglionic nerve activity

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