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Hi Everyone, I've been researching and researching non-stop and I've read through everyone's issues, every Dysautonomia website and it's all lead me to this post. I have a theory I'm working on and discussing with some Dysautonomia doctors. My theory only relates to our symptoms in a secondary nature because there are many primary causes and bundled all together it's causing different type of Dysautonomia. My theory unfortunately does not lead to a cure or even a cause but I believe it can help many of use with better treatment. My Theory: Our Dysautonomia symptoms are the result of imbalances in our blood pressure either systemically (through our whole circulatory system http://en.wikipedia.org/wiki/Systemic_disease), localized blood pressure imbalances (isolated to one organ at a time http://en.wikipedia.org/wiki/Localized_disease) and in some cases the imbalance of blood pressure disseminates to other organs (starts in one but spreads to others http://en.wikipedia.org/wiki/Disseminated_disease). Explanation: Our Autonomic Nervous systems (ANS) ( Para and Sympathetic) control our "flight or fight (FoF)" response but they also control our blood pressure using arterial sympathetic tonus which is separate from our FoF response. Our two ANS systems basically play a ping pong match to keep everything stable. Depending on what organ of the body either one (Symp or Para) constrict or dilate. I pasted examples below from Wikipedia. You will see Mast Cells, Blood Vessels, Digestive tract, Endo and Urinary, etc... Basically all Dysautonomia patient symptom areas. Okay so that's the basics, here is the details. I believe that at the heart of our Dysautonomia symptoms are our Arteries. Depending what primary disease, illness, complication, whatever... they are effecting the pressure in our arteries. This pressure is then causing our symptoms. And depend what primary issue you have it can affect our pressure systemically, locally or by diffusion. I believe there are two keys to lowering our symptoms. 1. We find the primary disease and we treat it. Unfortunately it seems that most of our primary disease have very poor treatment options and just are rarely curable and sometimes hardly manageable. 2. Is we locate our blood pressure issue, especially if it is localized and we get doctors to treat specific local blood pressure issues. Here are some of the local blood pressure issues I've found thus far. A) Pulmonary Pressure- Breathing issues, faintness http://en.wikipedia.org/wiki/Pulmonary_hypertension Intercranial Pressure- Brain issues- may cause dizziness, nausua, headaches http://en.wikipedia.org/wiki/Intracranial_pressure C) Renovascular hypertensions- Kidney issues- http://en.wikipedia.org/wiki/Renovascular_hypertension These are just a few of the more prevalent localized BP issues but there are others. Treatment is not great for BP issues because most medicines operate on a systemic level and go into our entire blood stream. And if a patient is has Pulmonary Hypertension but has systemic Hypotension then anti hypertension meds will help the breathing issues but exacerbate the systemic Hypotension. The hope is that they find meds that are selective to certain organs. They do have such meds for certain treatments and they are called "selective." Also note worthy is that hypertension is related to Mitochondrial issues, Nitric Oxide issues, endothelium issues and a few more vascular issues. And there are new CT Scans (which I posted) that will help diagnose they BP issues in the future... http://en.wikipedia.org/wiki/Autonomic_nervous_system Blood vessels Target Sympathetic (adrenergic) Parasympathetic (muscarinic) vascular smooth muscle in general α1: contracts; β2: relaxes M3: relaxes  renal artery α1: constricts --- larger coronary arteries α1 and α2: constricts  --- smaller coronary arteries β2:dilates  --- arteries to viscera α: constricts --- arteries to skin α: constricts --- arteries to brain α1: constricts  --- arteries to erectile tissue α1: constricts M3: dilates arteries to salivary glands α: constricts M3: dilates hepatic artery β2: dilates --- arteries to skeletal muscle β2: dilates --- Veins α1 and α2  : constricts β2: dilates --- Other Target Sympathetic (adrenergic) Parasympathetic (muscarinic) platelets α2: aggregates --- mast cells - histamine β2: inhibits --- Respiratory system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) smooth muscles of bronchioles β2: relaxes (major contribution) α1: contracts (minor contribution) M3: contracts The bronchioles have no sympathetic innervation, but are instead affected by circulating adrenaline  Nervous system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) Pupil dilator muscle α1: Contracts (causes mydriasis) - Iris sphincter muscle - M3: contracts (causes miosis) Ciliary muscle β2: relaxes (causes long-range focus) M3: contracts (causes short-range focus) Digestive system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) salivary glands: secretions β: stimulates viscous, amylase secretions α1: stimulates potassium secretions M3: stimulates watery secretions lacrimal glands (tears) β: stimulates protein secretion  --- juxtaglomerular apparatus of kidney β1: renin secretion --- parietal cells --- M1: Gastric acid secretion liver α1, β2: glycogenolysis, gluconeogenesis --- adipose cells β1, β3: stimulates lipolysis --- GI tract (smooth muscle) motility α1, α2, β2: decreases M3, (M1) : increases sphincters of GI tract α1, α2, β2: contracts M3: relaxes glands of GI tract no effect  M3: secretes Endocrine system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) pancreas (islets) α2: decreases insulin secretion from beta cells, increases glucagon secretion from alpha cells M3: increases secretion of both insulin and glucagon. adrenal medulla N (nicotinic ACh receptor): secretes epinephrine and norepinephrine --- Urinary system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) Detrusor urinae muscle of bladder wall β2: relaxes M3: contracts internal urethral sphincter α1: contracts M3: relaxes Reproductive system Target Sympathetic (adrenergic) Parasympathetic (muscarinic) uterus α1: contracts (pregnant) β2: relaxes (non-pregnant) --- genitalia α1: contracts (ejaculation) M3: erection Integumentary system Target Sympathetic (muscarinic and adrenergic) Parasympathetic sweat gland secretions M: stimulates (major contribution); α1: stimulates (minor contribution) --- arrector pili α1: stimulates --- References
Here is the full abstract of the study http://hyper.ahajournals.org/content/51/2/412.full . Many of us are believed to have Mitochondrial Deficiencies and we are not sure if it is primary or secondary. But it could play a role in a lot our fatigue and other symptoms. I also have a theory that many of our symptoms are a result of what I call localized hypertension. Just like some of us have Orthostatic BP flucuations, I believe some other mechanism make our BP irregular in different parts of our bodies. And if one of us have a symptom that bothers us more it's because of the irregularity is localized to an area of the body that causes that type of symptom. This all ties into autonomic dysfunction. Even if one of has dysfunction because of a completely different illness than from another person, treating this local fluctuation might be a key, might, just a theory so far... Mitochondrial Dysfunction Mitochondrial Dysfunction in the Hypertensive Rat Brain Respiratory Complexes Exhibit Assembly Defects in Hypertension The central nervous system plays a critical role in the normal control of arterial blood pressure and in its elevation in virtually all forms of hypertension. Mitochondrial dysfunction has been increasingly associated with the development of hypertension. Perspectives The central nervous system plays a critical role in the normal control of arterial blood pressure and in its elevation in virtually all forms of hypertension. Our findings suggest that, in already-hypertensive SHRs, the brain respiratory complexes exhibit previously unknown assembly defects. These defects impair the function of the mitochondrial respiratory chain. This mitochondrial dysfunction localizes to the brain stem and is, therefore, likely to contribute to the development, as well as to pathophysiological complications, of hypertension. Interestingly, mitochondrial dysfunction in the central nervous system has been extensively investigated for several neurodegenerative diseases, including vascular dementia, Alzheimer’s, Huntington’s, and Parkinson’s disease.34–37 It is striking that the dysfunction that occurs in these diseases shares many molecular commonalities with that found in the current research in the context of hypertension. Future research should further explore the emerging link among hypertension, mitochondrial dysfunction, and neurodegeneration and the cause-effect relationships.