Models of Hypertension in Aging

Reckelhoff, Jane F.; Cardozo, Licy L. Yanes; Fortepiani, Maria Lourdes Alarcon

doi:10.1016/b978-0-12-811353-0.00052-x

Cited by 5 publications

(3 citation statements)

References 105 publications

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“…Hypertension triggers are a series of initial compensatory changes that contribute towards heart failure while ageing (Drazner, 2011; Santos & Shah, 2014). Key studies of ageing in hypertension are performed mainly on rodents since these animals have relatively short life spans, are inexpensive to purchase and maintain, and can be easily manipulated (Reckelhoff et al, 2018). Noteworthy, the normal blood pressure in healthy rats is the same as in humans.…”

Section: Discussionmentioning

confidence: 99%

“…Juvenile spontaneously hypertensive rats before sexual maturity are prehypertensive in which the blood pressure only starts to climb; meanwhile, the adult spontaneously hypertensive rats, sexually matured animals of this breed, are generally considered as stably hypertensive with systolic blood pressure exceeding over 150 mm Hg (Adams et al, 1989; Boluyt et al, 1995; de Rezende et al, 2021; Doggrell & Brown, 1998; Okamoto & Aoki, 1963; Panzenhagen et al, 2019). The age for persistent hypertension group was based on life span of used breeds which is 1.5–2.5 years for spontaneously hypertensive rats and 2.5–3 years for Wistar–Kyoto rats (Reckelhoff et al, 2018).…”

Section: Methodsmentioning

confidence: 99%

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Neurochemical alterations of intrinsic cardiac ganglionated nerve plexus caused by arterial hypertension developed during ageing in spontaneously hypertensive and Wistar Kyoto rats

et al. 2023

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The acknowledged hypothesis of the cause of arterial hypertension is the emerging disbalance in sympathetic and parasympathetic regulations of the cardiovascular system. This disbalance manifests in a disorder of sustainability of endogenous autonomic and sensory neural substances including calcitonin gene‐related peptide (CGRP). This study aimed to examine neurochemical alterations of intrinsic cardiac ganglionated nerve plexus (GP) triggered by arterial hypertension during ageing in spontaneously hypertensive rats of juvenile (prehypertensive, 8–9 weeks), adult (early hypertensive, 12–18 weeks) and elderly (persistent hypertensive, 46–60 weeks) age in comparison with the age‐matched Wistar–Kyoto rats as controls. Parasympathetic, sympathetic and sensory neural structures of GP were analysed and evaluated morphometrically in tissue sections and whole‐mount cardiac preparations. Both the elevated blood pressure and the evident ultrasonic signs of heart failure were identified for spontaneously hypertensive rats and in part for the aged control rats. The amount of adrenergic and immunoreactive to CGRP neural structures was increased in the adult group of spontaneously hypertensive rats along with the significant alterations that occurred during ageing. In conclusion, the revealed chemical alterations of GP support the hypothesis about the possible disbalance of efferent and afferent heart innervation and may be considered as the basis for the emergence and progression of arterial hypertension and perhaps even as a consequence of hypertension in the aged spontaneously hypertensive rats. The determined anatomical changes in the ageing Wistar–Kyoto rats suggest this breed being as inappropriate for its use as control animals for hypertension studies in older animal age.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Neurochemical alterations of intrinsic cardiac ganglionated nerve plexus caused by arterial hypertension developed during ageing in spontaneously hypertensive and Wistar Kyoto rats

et al. 2023

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“…The Spontaneously hypertensive rat (SHR) is currently the best-validated animal model of ADHD based on behavioral, genetic, and neurobiological data [ 42 – 44 ]. SHRs are normotensive at birth and gradually develop increases in blood pressure beginning at 6–7 weeks of age and reach a stable level of hypertension by 17–19 weeks of age [ 45 – 47 ]. SHR shows overactivity under the control of a fixed-interval operant reinforcement schedule [ 42 , 48 ], increased behavioral variability [ 49 ] and problems with cognitive impulsiveness [ 50 ] similar to that of ADHD children.…”

Section: Introductionmentioning

confidence: 99%

The mesocortical dopaminergic system cannot explain hyperactivity in an animal model of attention deficit hyperactivity disorder (ADHD)- Spontaneously hypertensive rats (SHR)

Gungor Aydin,

Adiguzel

2023

Lab Anim Res

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Background Attention deficit hyperactivity disorder (ADHD) is one of the most prevalent neuropsychiatric disorders with morphological brain abnormalities. There is a growing body of evidence that abnormalities in the dopaminergic system may account for ADHD pathogenesis. However, it is not clear whether the dopaminergic system is hyper or hypoactive. To determine whether the DA neurons and/or axons deficiency might be the cause of the postulated dopaminergic hypofunction in spontaneously hypertensive rats (SHR, animal model of ADHD), this study examined the dopaminergic neurons and fibers in the brain tissues of SHRs and Wistar Kyoto rats (WKY, control animals). Here, we performed immunohistochemical tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH) staining on brain sections collected on juveniles from SHR and WKY. Moreover, behavioral testing to examine the hyperactivity in the open field area was also elucidated. Results The mesocortical dopaminergic system appears to be normal in juvenile SHR, as suggested by (i) no alteration in the area density of TH-immunoreactive (TH-ir) dopaminergic neurons in the ventral tegmental area (VTA), (ii) no alterations in the volume density of TH-ir fibers in layer I of the prelimbic (PrL) subregion of medial PFC (mPFC), (iii) no alteration in the percentage of TH-ir dopaminergic fibers in layer I of the PrL subregion of mPFC as revealed by TH and/or DBH immunoreactivity. Furthermore, the SHR showed increased locomotor activity than WKY in the open field test. Conclusions The demonstration of no alteration in mesocortical dopaminergic neurons and fiber in SHR raises some concern about the position of SHR as an animal model of the inattentive subtype of ADHD. However, these results strengthen this strain as an animal model of hyperactive/impulsive subtype ADHD for future studies that may elucidate the underlying mechanism mediating hyperactivity and test various treatment strategies.

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Upregulation of Glutamatergic Receptors in Hippocampus and Locomotor Hyperactivity in Aged Spontaneous Hypertensive Rat

Yen

Liu

Chu³

2021

Cell Mol Neurobiol

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Models of Hypertension in Aging

Cited by 5 publications

References 105 publications

Neurochemical alterations of intrinsic cardiac ganglionated nerve plexus caused by arterial hypertension developed during ageing in spontaneously hypertensive and Wistar Kyoto rats

Neurochemical alterations of intrinsic cardiac ganglionated nerve plexus caused by arterial hypertension developed during ageing in spontaneously hypertensive and Wistar Kyoto rats

The mesocortical dopaminergic system cannot explain hyperactivity in an animal model of attention deficit hyperactivity disorder (ADHD)- Spontaneously hypertensive rats (SHR)

Upregulation of Glutamatergic Receptors in Hippocampus and Locomotor Hyperactivity in Aged Spontaneous Hypertensive Rat

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