Gland In Hypertension Research Articles

Morphological and histochemical changes in the pituitary gland in atherosclerosis and hypertension

In the morphological study of the endocrine glands in hypertension and atherosclerosis, much attention is usually paid to the pituitary gland, since the greatest importance is attached to its functional disorders in these diseases (G. Cushing, A.T. Rassmussen, A.A. Waldman, I.S. Weinberg and M. K-Dal, E. V. Uranova, E. A. Savina, Yu. I. Miklyaev and others).

Analyses of circRNA and mRNA profiles in the submandibular gland in hypertension

The aim of this study was to elucidate the roles played by circular RNAs (circRNAs) in the mechanism underlying submandibular gland (SMG) dysfunction in hypertension. We employed RNA-seq to analyze the circRNA and mRNA expression profiles of SMGs. Seventy-five differentially expressed (DE) circRNAs and 691 DE mRNAs were determined to be significantly altered in spontaneously hypertensive rats. Altered mRNAs were primarily related to the immune system and immune response. Eight circRNAs were selected for further analysis. Cell adhesion molecules were determined to be the most strongly enriched pathway through analysis of DE mRNAs, the coding noncoding gene co-expression (CNC) network and the competitive endogenous RNA (ceRNA) network. The salivary secretion pathway was observed to be notably enriched through analysis of the ceRNA network. These results suggest that the crosstalk among circRNAs may play a crucial role in the development of SMG dysfunction in hypertension.

LncRNA and mRNA expression profiles and functional networks of hyposalivation of the submandibular gland in hypertension

Hyposalivation is a complication of hypertension. However, little is known about the role of long non-coding RNAs (lncRNAs) in salivary glands in hypertension. This study aimed to compare the lncRNA and mRNA expression profiles between spontaneous hypertension rats (SHRs) and Wistar-Kyoto (WKY) rats through microarray analysis and apple bioinformatics methods to analyse their potential roles in hyposalivation. The differentially expressed (DE) lncRNAs and mRNAs were confirmed by quantitative real-time PCR (qRT-PCR). Compared with WKY rats, 225 DE lncRNAs and 473 DE mRNAs were identified in the SMG of SHRs. The pathway analyses of DE mRNAs showed that inflammatory mediator regulation of transient receptor potential channels was involved in hyposalivation in SHRs. Ten DE lncRNAs were chosen for further research. A coding-non-coding gene co-expression (CNC) network and competing endogenous RNA (ceRNA) network analysis revealed that the potential functions of these 10 DE lncRNAs were closely connected with the processes of the immune response. This study showed abundant DE lncRNAs and mRNAs in hypertensive SMGs. Furthermore, our results indicated strong associations between the immune response and hyposalivation and showed the potential of immune-related genes as novel and therapeutic targets for hyposalivation.

Proteomic analysis reveals an impaired Ca2+/AQP5 pathway in the submandibular gland in hypertension

Hypertension is a systemic disorder that affects numerous physiological processes throughout the body. Improper sodium transport is a common comorbidity of hypertension, and sodium transport is also critical for maintaining the secretion of submandibular glands, whether the function of submandibular glands is affected by hypertension remains unclear. To determine whether hypertension induces changes in the protein expression of submandibular glands, we compared the proteome of submandibular glands from 14-week-old spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats using LC-MS/MS. The results revealed that 95 proteins displayed different levels of expression between the submandibular glands from the SHRs and WKYs. Among these, 35 proteins were more abundant, and 60 proteins were less abundant in the SHR compared with the WKY rats. Specifically, aquaporin 5 and parvalbumin, which are correlated with water transport and intracellular Ca2+ signal transduction, were verified to exhibit differences in protein abundance. Impaired Ca2+ response to carbachol was confirmed in the acinar cells from SHRs, and hyposecretion by the submandibular glands was further confirmed by in vivo saliva collection. In conclusion, the proteomic analysis of the submandibular glands of SHRs revealed novel changes in protein abundance that provides possible mechanisms connecting hypertension and hyposecretion in submandibular glands.

The role of the adrenal gland in hypertension.

The adrenal gland plays a unique role in the etiology of many forms of hypertension. Recognizable syndromes of adrenal gland disease in which hypertension is observed can be identified and localized to each of the functional and histologic divisions of the adrenal cortex and medulla. The diagnosis of the various syndromes of adrenal hormone excess is a critically important first step in the successful identification, localization, and treatment of adrenal gland disorders.

Computed tomography of the adrenal gland in hypertension.

Computed tomography (CT) is a rapid, safe, and accurate method to detect or exclude the presence of an adrenal mass. CT should be the first imaging procedure in patients with biochemical evidence of pheochromocytoma. Cushing’s syndrome, or primary aldosteronism.

Present status of the pathology of the adrenal gland in hypertension

Present status of the pathology of the adrenal gland in hypertension

Observations on the Hypophyseal Area in Hypertension

The problem of the etiology of hypertension is a complex one, and one that is far from being solved. Although recent studies have greatly modified our views regarding the probable pathogenesis of essential hypertension, and have advanced our understanding of the problem considerably, no etiological factor has been established which will explain all cases. Renal hypertension was induced by Goldblatt (1) in animals by clamping the renal artery, producing a renal ischemia. Renal ischemia has also been produced by numerous other devices, such as ureteral obstruction, constriction of the kidney by a cellophane membrane, partial excision of the kidney, and by experimental nephritis. The renin pressor mechanism which develops as a result of the renal ischemia is responsible for the hypertension in the experimental animal. The evidence that this mechanism is responsible for essential human hypertension is not conclusive. It may account for some cases, but it does not explain the etiology in all cases, nor does it exclude other factors as the primary cause in some and an accessory cause in others. The view that some extrarenal factor may be responsible for the initial renal ischemia has not received much support. The part played by the glands of internal secretion has been studied by Page (2), Goldblatt (3), and others. Hypophysectomy does not prevent the development of experimental renal hypertension, and Goldblatt believes that the pituitary is not important in the mechanism of hypertension of this type. He found, however, that high blood pressure was not well maintained in the absence of the gland. Excision of both gonads, thyroid, and pancreas is also without effect on the development of this kind of hypertension. The only gland definitely implicated is the adrenal. Bilateral adrenalectomy, with consequent removal of adrenal cortical tissue, interferes with the development and maintenance of experimental renal hypertension unless substitution therapy is maintained. It is well known, however, that tumors producing over-activity of the pituitary or the adrenal glands are responsible for the occurrence of high blood pressure and that hypofunction of these glands is characterized by hypotension. Pheochromocytoma and adrenal carcinoma are the most common lesions of the adrenal glands associated with hypertension. Tumors of the pituitary gland may play a role in the mechanism of high blood pressure, the most common being the basophile adenoma or infiltration characteristic of Cushing's syndrome. Acromegaly is often accompanied by hypertension, while Simmond's disease or atrophy of the pituitary usually leads to marked hypotension. The mechanism of these changes, however, is not clear. Renewed interest in the role of the pituitary gland in hypertension has been stimulated by the recent work of Pendergrass, Griffith, and associates.

Differential cell counts of the pituitary gland in hypertension and endocrine disturbances

Differential cell counts of the pituitary gland in hypertension and endocrine disturbances